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BMSC-Exos affect inflammation and oxidative stress in DR rats by modulating the TLR4/NF-κB signaling pathway 认领 引用
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作者 Wang Qin Zeng Feng +2 位作者 Liu Wei Huang Hao Wang Haizhi 《国际眼科杂志》 CAS 2026年第8期1307-1315,共9页
AIM:To investigate the therapeutic effects of bone marrow mesenchymal stem cell-derived exosomes(BMSC-Exos)on diabetic retinopathy(DR)in rats,with a focus on their ability to modulate oxidative stress and inflammatory... AIM:To investigate the therapeutic effects of bone marrow mesenchymal stem cell-derived exosomes(BMSC-Exos)on diabetic retinopathy(DR)in rats,with a focus on their ability to modulate oxidative stress and inflammatory responses through the TLR4/NF-κB signaling pathway.METHODS:Streptozotocin(STZ)-induced diabetic Sprague-Dawley(SD)rats were randomly divided into four groups:Group 1[normal+phosphate-buffered saline(PBS)],Group 2(normal+Exos),Group 3(DR+PBS),and Group 4(DR+Exos).At the 8 th week after modeling,BMSC-Exos or PBS were injected intravitreally.Retinal tissues were collected at the 16 th week for histological analysis[hematoxylin and eosin(HE)staining],apoptosis detection(TUNEL).Oxidative stress markers[8-OHdG,superoxide dismutase(SOD),and glutathione(GSH)]were assessed,and inflammatory cytokines[enzyme-linked immunosorbent assay(ELISA)for interleukin(IL)-6 and tumor necrosis factor-alpha(TNF-α)],and molecular profiling[quantitative polymerase chain reaction(qPCR)for TLR4,NF-κB,and VEGF]were measured.RESULTS:The BMSC-Exos treatment significantly suppressed the activation of the TLR4/NF-κB pathway in DR rats(P<0.01),which was accompanied by reduced retinal vascular leakage(Evans blue assay,P<0.001),decreased apoptosis(TUNEL,P<0.05),and attenuated oxidative stress(elevated SOD and GSH,reduced 8-OHdG,P<0.05).The levels of inflammatory cytokines(IL-6 and TNF-α)were markedly decreased(P<0.01).CONCLUSION:BMSC-Exos alleviate DR by suppressing the TLR4/NF-κB axis,thus reducing oxidative damage,inflammation,and microvascular dysfunction.This research offers a novel therapeutic approach for early-stage DR. 展开更多
关键词 bone marrow mesenchymal stem cells exosomes TLR4/NF-κB signaling pathway oxidative stress
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Gastrodin attenuates dextran sulfate sodium-induced colitis in mice via modulating gut microbiota and inhibiting NF-κB signaling pathway 认领 引用 被引量：2
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作者 Xinyi Gao Xianjun Liu +8 位作者 Xianglong Meng Mingchuan Wang Mengyuan Wang Boyao Sun Chengxuan Jia Jintian Gao Chengyi Xu Hao Li Yang Jiang 《Food Science and Human Wellness》 SCIE CAS CSCD 2025年第9期3617-3635,共19页
Gastrodin(GAS),the principal bioactive composition of Gastrodia elata Blume,has potential for pharmaceutical applications.Several studies in recent years have shown that GAS may enhance neurotrophic benefits,reduce in... Gastrodin(GAS),the principal bioactive composition of Gastrodia elata Blume,has potential for pharmaceutical applications.Several studies in recent years have shown that GAS may enhance neurotrophic benefits,reduce inflammation,and act as an antioxidant.In this study,we sought to identify the molecular mechanisms underlying the protective benefits of GAS against colitis induced by dextran sodium sulfate(DSS)in mice.GAS(200 mg/kg)significantly ameliorated the severity of colitis in mice caused by DSS,as evidenced by an increase in colon length,a reduction in disease activity index,a decrease in tissue damage,and a reduction in body weight loss.Additionally,GAS inhibited DSS-induced hyperactivation of inflammation-related NF-κB signaling pathways to reduce the production of inflammatory mediators,thereby mitigating the inflammatory response in mice.Furthermore,the administration of GAS restored the function of the gastrointestinal barrier by increasing the count of goblet cells,as well as the levels of tight junction associated proteins,including Zonula occludens-1(ZO-1),Occludin,and Claudin-3.GAS also influenced the overall richness of the gut microbiota,as shown by 16S rRNA sequencing analysis,consequently boosting the proliferative rate of probiotic species,such as Lachnospiraceae and Muribaculaceae,while reducing the richness of harmful bacteria including Escherichia_Shigella,Enterobacteriaceae,Bacteroidaceae,and Bacteroides.GAS(200 mg/kg)alleviated ulcerative colitis(UC)by modulating gut dysbiosis,as demonstrated by a fecal microbial transplantation(FMT)test.Furthermore,inflammatory damage induced by lipopolysaccharide(LPS)was averted in RAW264.7 cells by GAS administration,hence preventing the NF-κB signaling pathway from being activated in these experimental conditions conducted in vitro.Overall,the data indicate that GAS treatment effectively reduces colitis caused by DSS by regulating gut microbiota,suppressing inflammation,and preserving the mucosal barrier integrity. 展开更多
关键词 Gastrodin Intestinal barrier Ulcerative colitis NF-κB signaling pathway Gut microbiota
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Dietary hydrolysable tannin improves intestinal health of largemouth bass(Micropterus salmoides):insights from NF-κB signaling pathway and arachidonic acid metabolism 认领 引用
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作者 Manqi Yang Dahai Jiang +9 位作者 Zhangyi Xiao Weibin Lai Kai Chen Shuwen Xu Yuanyi Zuo Liangliang Zhang Liming Lu Xiaoping Rao Chunxiao Zhang Jianchun Jiang 《Journal of Animal Science and Biotechnology》 SCIE CAS CSCD 2025年第6期2966-2985,共20页
Background To more effectively address the scarcity resources and elevated costs associated with fishmeal(FM),the utilization of cottonseed protein concentrate(CPC)as an alternative in aquaculture feeds has become inc... Background To more effectively address the scarcity resources and elevated costs associated with fishmeal(FM),the utilization of cottonseed protein concentrate(CPC)as an alternative in aquaculture feeds has become increasingly prevalent.However,high levels of CPC substitution for FM have been reported to suppress the growth of fish and impair intestinal health.Hydrolysable tannin(HT)has been reported to exhibit biological activities such as antiinflammatory and antioxidant activities,but whether the HT can generate positive biological effects on the intestinal health of largemouth bass(Micropterus salmoides)remains unknown.Largemouth bass(initial weight:6.03±0.01 g)were subjected to an 8-week feeding trial with three different diets:a basic diet(named as the NC),a high CPC diet(in which CPC replaced 75%of the FM protein in the NC diet,named as the HC),and an additive diet(1.25 g/kg of the HT was added to the HC diet,named as the HCH)to explore the potential benefits of HT on intestinal health.Results The HC treatment significantly reduced the weight gain rate of fish,increased the feed conversion ratio,and induced intestinal inflammation.However,the HCH treatment could alleviate the adverse impacts of the HC diet,as evidenced by the promotion of growth and feed utilization,increased activity of digestive enzymes and antioxidant capacities,downregulated expression of pro-inflammatory factors,and maintenance of the integrity of intestinal barrier.Metabolomic analysis revealed that HCH treatment could reduce the pro-inflammatory active substances produced by arachidonic acid metabolism,including prostaglandin F2α(PGF2α)and leukotriene B4(LTB4).Transcriptomic results indicated that dietary HT might alleviate intestinal inflammation by suppressing the activation of the NF-κB signaling pathway.Furthermore,correlation analysis demonstrated that the metabolites PGF2αand LTB4,derived from arachidonic acid,exhibited a significant positive correlation with the expression of genes associated with proinflammatory responses within the NF-κB signaling pathway.Conclusions The study indicates that the HT mitigates the growth retardation and intestinal inflammation resulting from the HC diet on largemouth bass. 展开更多
关键词 Arachidonic acid metabolism Hydrolysable tannin Intestinal inflammation Largemouth bass NF-κB signaling pathway Plant-based protein source
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Shikonin shows retinoprotective effects in diabetic rats via modulating the Nrf2/HO-1 and NF-κB signaling pathways 认领 引用
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作者 Xia Ren Meng-Meng Zhao Juan Du 《Asian Pacific Journal of Tropical Biomedicine》 SCIE CAS 2025年第8期342-352,I0002-I0006,共11页
Objective:To examine the effect of shikonin against streptozotocin(STZ)-induced diabetic retinopathy in rats and elucidate the underlying mechanisms.Methods:Intraperitoneal administration of STZ(65 mg/kg)was used for ... Objective:To examine the effect of shikonin against streptozotocin(STZ)-induced diabetic retinopathy in rats and elucidate the underlying mechanisms.Methods:Intraperitoneal administration of STZ(65 mg/kg)was used for the induction of diabetic retinopathy in rats.Rats received oral administration of shikonin(10,20,and 30 mg/kg).The blood glucose level,insulin,body weight,and organ weight were estimated.Advanced glycation end products(AGEs)levels in serum and lens as well as protein carbonyl content of the lens were determined.The parameters related to oxidative stress and inflammation,and the levels of nuclear factor erythroid 2-related factor 2(Nrf2),heme oxygenase-1(HO-1),intercellular adhesion molecule-1(ICAM-1),and vascular cell adhesion molecule 1(VCAM-1)were also measured.In addition,quantitative RT-PCR was performed to determine the mRNA expressions.Results:Shikonin treatment decreased glucose level and boosted insulin level,along with an increase in body weight and improved organ weight.It also lowered O2•−,ONOO−,serum and lens AGEs,and protein carbonyl content.Furthermore,shikonin treatment significantly alleviated oxidative stress and inflammation,as evidenced by reduced malonaldehyde,nitric oxide,tumor necrosis factor-α(TNF-α),interleukin-1β(IL-1β),IL-6,cyclooxygenase-2,prostaglandin E2,protein carbonyl content,and nuclear factor kappa-B,and increased superoxide dismutase,glutathione,catalase,and glutathione peroxidase.Markedly decreased levels of ICAM-1 and VCAM-1,as well as heightened levels of Nrf2 and HO-1,were noticed after treatment with shikonin.Furthermore,the mRNA expressions of TNF-α,IL-1β,IL-6,ICAM-1,VCAM-1,RAGE,collagenⅣ,and fibronectin were significantly downregulated.Conclusions:Shikonin exhibits protective effects against STZ-induced diabetic retinopathy in rats via modulating the Nrf2/HO-1 and NF-κB signaling pathways. 展开更多
关键词 Diabetic retinopathy Shikonin Serum AGEs Nrf2/HO-1 NF-κB signaling pathway
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Mesalazine alleviated the symptoms of spontaneous colitis in interleukin-10 knockout mice by regulating the STAT3/NF-κB signaling pathway 认领 引用 被引量：5
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作者 Qian Chen Ya-Li Zhang +1 位作者 Yong-Quan Shi Lie Zheng 《World Journal of Gastroenterology》 SCIE CAS 2025年第7期88-97,共10页
BACKGROUND Excessive endoplasmic reticulum(ER)stress in intestinal epithelial cells can lead to damage to the intestinal mucosal barrier,activate the signal transducer and activator of transcription 3(STAT3)uclear fac... BACKGROUND Excessive endoplasmic reticulum(ER)stress in intestinal epithelial cells can lead to damage to the intestinal mucosal barrier,activate the signal transducer and activator of transcription 3(STAT3)uclear factor kappa B(NF-κB)signaling pathway,and exacerbate the inflammatory response,thus participating in the pathogenesis of ulcerative colitis(UC).Mesalazine is a commonly used drug in the clinical treatment of UC.However,further studies are needed to determine whether mesalazine regulates the ER stress of intestinal epithelial cells,downregulates the STAT3/NF-κB pathway to play a role in the treatment of UC.AIM To study the therapeutic effects of mesalazine on spontaneous colitis in interleukin-10(IL-10)-/-mice.METHODS The 24-week-old IL-10-/-mice with spontaneous colitis were divided into the model group and the 5-amino salicylic acid group.Littermates of wild-type mice of the same age group served as the control.There were eight mice in each group,four males and four females.The severity of symptoms of spontaneous colitis in IL-10-/-mice was assessed using disease activity index scores.On day 15,the mice were sacrificed.The colon length was measured,and the histopathological changes and ultrastructure of colonic epithelial cells were detected.The protein expressions of STAT3,p-STAT3,NF-κB,IκB,p-IκB,and glucoseregulated protein 78 were identified using Western blotting.The STAT3 and NF-κB mRNA expressions were identified using real-time polymerase chain reaction.The glucose-regulated protein 78 and C/EBP homologous protein expressions in colon sections were detected using immunofluorescence.RESULTS Mesalazine reduced the symptoms of spontaneous colitis in IL-10 knockout mice and the histopathological damage of colonic tissues,and alleviated the ER stress in epithelial cells of colitis mice.Western blotting and quantitative real-time polymerase chain reaction results showed that the STAT3/NF-κB pathway in the colon tissue of model mice was activated,suggesting that this pathway was involved in the pathogenesis of UC and might become a potential therapeutic target.Mesalazine could down-regulate the protein expressions of p-STAT3,NF-κB and p-IκB,and down-regulate the mRNA expression of STAT3 and NF-κB.CONCLUSION Mesalazine may play a protective role in UC by reducing ER stress by regulating the STAT3/NF-κB signaling pathway. 展开更多
关键词 Mesalazine Ulcerative colitis Interleukin-10-/-mice Signal transducer and activator of transcription 3uclear factor kappa B signaling pathway Endoplasmic reticulum stress Inflammatory bowel disease
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The Regulatory Effect of miR-146a Overexpression on Corneal Inflammatory Response in a Mouse Model of Dry Eye Disease and Its Relationship with the IRAK1/TRAF6/NF-κB Signaling Pathway 认领 引用
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作者 ZHONG Jun-mu LIN Xiao-yan +1 位作者 LAI Mei-hua LIN Cui-rong 《Chinese Journal of Biomedical Engineering(English Edition)》 CAS 2025年第2期69-77,共9页
Objective:To investigate the regulatory effect of miR-146a overexpression on corneal inflammatory response in a mouse model of dry eye,and to analyze its relationship with the IRAK1/TRAF6/NF-кB signaling pathway.Meth... Objective:To investigate the regulatory effect of miR-146a overexpression on corneal inflammatory response in a mouse model of dry eye,and to analyze its relationship with the IRAK1/TRAF6/NF-кB signaling pathway.Methods:A total of 50 SPF-grade BALB/c mice were randomly divided into five groups,with10 mice in each group.Except for the control group,the other four groups were treated with 0.2%benzalkonium chloride(BAC)solution in both eyes to construct a dry eye model.After successful modeling,the control group and model group received NC agomir;the miR antagonist group received miR-146a antagomir;the miR agonist group received miR-146a agomir;and the pathway agonist group received miR-146a agomir+NF-κB activator 2.After four weeks of treatment,the expressions levels of miR-146a,inflammatory factors,and IRAK1/TRAF6/NF-κB signaling pathway proteins were observed and compared among the five groups.Results:After four weeks of treatment,there was a statistically significant difference in the relative expression of miR-146a in the five groups(F=61.058,P<0.001),which was significantly higher in the miR agonist group than in the other four groups.After4 weeks of treatment,there were statistically significant differences in the expression levels of IL-1β,IL-6,IL-8 and TNF-αin the five groups(F=84.757,103.658,55.477,46.762;P<0.001).After four weeks of treatment,there were statistically significant differences in the protein expression levels of IRAK1,TRAF6,NF-κB and IκBαin the five groups(F=62.975,77.173,67.108,29.381;P<0.001),except for the control group,the expression levels of IRAK1,TRAF6 and NF-κB proteins in the miR agonist group were significantly lower than those in the other three groups,and the expression levels of IκBαprotein were significantly higher than those in the other three groups.Conclusion:Overexpression of miR-146a can negatively regulate corneal inflammatory response in dry eye mice through the IRAK1/TRAF6/NF-κB signaling pathway,which can provide new insights for the clinical treatment of dry eye disease. 展开更多
关键词 dry eye disease miR-146a IRAK1/TRAF6/NF-κB signaling pathway inflammatory response
Effect of warming yang and supplementing kidney moxibustion therapy on the NF-κB signaling pathway of vascular dementia rats 认领 引用 被引量：10
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作者 Wanli ZHU Kun YANG +2 位作者 Shengchao CAI Ying WANG Xiaoge SONG 《World Journal of Acupuncture-Moxibustion》 CAS CSCD 2018年第1期44-49,I0006,I0007,共6页
Objective： To observe the effect of warming yang and supplementing kidney moxibustion therapy on the behavioristics and the expression levels of hippocampal IL-1β, TNF-α and NF-κB related genes and proteins of vas... Objective： To observe the effect of warming yang and supplementing kidney moxibustion therapy on the behavioristics and the expression levels of hippocampal IL-1β, TNF-α and NF-κB related genes and proteins of vascular dementia（VD） rats, and to explore the mechanism of warming yang and supplementing kidney moxibustion therapy in inhibiting VD inflammatory response. Methods Seventy-eight SD rats, except 10 rats as sham operation group（group A）, were established into VD models by applying the ischemia reperfusion method in bilateral common carotid arteries. 30 models were successful and were randomly divided into model group（group B）, moxibustion group（group C） and western medication group（group D）, with 10 rats in each group. After modeling, suspended moxibustion was conducted at ＂Dàzhuī（大椎GV 14）＂,＂Mìngmén（命门GV 4）＂ and ＂Guānyuán（关元CV 4）＂ of the rats in group C for15 minime. The intervention was performed for once a day, and intervention for 4 consecutive weeks was needed. Intragastric administration with nimodipine（2 mgkg-1d-1） was carried out in the rats in group D for 4 consecutive weeks. Morris water maze test was adopted for behavioral test in the rats in each group. HE staining was conducted in order to observe the pathological changes. RT-qPCR method and Western blot method were used for detecting the expression levels of hippocampal IL-1β, TNF-αand NF-κB related genes and proteins.Results： After modeling, the Morris water maze escape latency of rats in operation groups was obviously longer than that in group A（P〈0.05）. According to HE staining results, the arrangement of neurons in group B was incompact, the cell membranes were undefined, the cytoplasm was heterogeneous, karyopyknosis was found, the amount of necrosis increased, and the number of inflammatory cells significantly increased. Compared with group B, the number of inflammatory cells significantly reduced in group C and group D, and the amount of neuron necrosis also reduced. After intervention, compared with group B, the expression levels of TNF-a, p-IκB and NF-κBp65 mRNA in the hippocampal of the rats in group C and group D significantly decreased（all P〈0.05）, compared with group B, the expression levels of IL-1β, TNF-α and NF-κBp65 mRNA in the hippocampal of rats in group C and group D also significantly decreased（all P〈0.05）.Conclusion： Warming yang and supplementing kidney moxibustion therapy may inhibit the NF-κB signaling pathway and reduce the inflammatory response through lowering the expression levels of IL-1β,TNF-α and NF-κB mRNA in the brain, thus achieving the purpose of treating VD. 展开更多
关键词 Moxibustion Vascular dementia rats Inflammatory response NF-κB signaling pathway Hippocampal
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Acupuncture at Back-Shu point improves insomnia by reducing inflammation and inhibiting the ERK/NF-κB signaling pathway 认领 引用 被引量：11
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作者 Ming-Ming Zhang Jing-Wei Zhao +2 位作者 Zhi-Qiang Li Jing Shao Xi-Yan Gao 《World Journal of Psychiatry》 SCIE 2023年第6期340-350,共11页
BACKGROUND Insomnia is a disease where individuals cannot maintain a steady and stable sleep state or fail to fall asleep.Western medicine mainly uses sedatives and hypnotic drugs to treat insomnia,and long-term use i... BACKGROUND Insomnia is a disease where individuals cannot maintain a steady and stable sleep state or fail to fall asleep.Western medicine mainly uses sedatives and hypnotic drugs to treat insomnia,and long-term use is prone to drug resistance and other adverse reactions.Acupuncture has a good curative effect and unique advantages in the treatment of insomnia.AIM To explore the molecular mechanism of acupuncture at Back-Shu point for the treatment of insomnia.METHODS We first prepared a rat model of insomnia,and then carried out acupuncture for 7 consecutive days.After treatment,the sleep time and general behavior of the rats were determined.The Morris water maze test was used to assess the learning ability and spatial memory ability of the rats.The expression levels of inflammatory cytokines in serum and the hippocampus were detected by ELISA.qRTPCR was used to detect the mRNA expression changes in the ERK/NF-κB signaling pathway.Western blot and immunohistochemistry were carried out to evaluate the protein expression levels of RAF-1,MEK-2,ERK1/2 and NF-κB.RESULTS Acupuncture can prolong sleep duration,and improve mental state,activity,diet volume,learning ability and spatial memory.In addition,acupuncture increased the release of 1L-1β,1L-6 and TNF-αin serum and the hippocampus and inhibited the mRNA and protein expression of the ERK/NF-κB signaling pathway.CONCLUSION These findings suggest that acupuncture at Back-Shu point can inhibit the ERK/NF-κB signaling pathway and treat insomnia by increasing the release of inflammatory cytokines in the hippocampus. 展开更多
关键词 ERK/NF-κB signaling pathway Acupuncture Insomnia Inflammation Acupuncture at Back-Shu point Traditional Chinese medicine
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Ethnopharmacological study on Adenosma buchneroides Bonati inhibiting inflammation via the regulation of TLR4/MyD88/NF-κB signaling pathway 认领 引用 被引量：4
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作者 Yuru Shi Xiaoqian Zhang +1 位作者 Shengji Pei Yuhua Wang 《Natural Products and Bioprospecting》 CSCD 2024年第1期656-667,共12页
Adenosma buchneroides Bonati,also known as fleagrass,is an important medicinal plant used by the Akha(Hani)people of China for treating inflammation-related skin swelling,acne,and diarrhoea,among other conditions.In t... Adenosma buchneroides Bonati,also known as fleagrass,is an important medicinal plant used by the Akha(Hani)people of China for treating inflammation-related skin swelling,acne,and diarrhoea,among other conditions.In this study,we aimed to evaluate the anti-inflammatory activities and explore the molecular mechanisms of fleagrass on treating skin swelling and acne.The results demonstrated that fleagrass inhibited the enzymatic activities of 5-LOX and COX-2 in vitro,and decreased the release of NO,IL-6,TNF-α,and IL-10 in the LPS-induced RAW264.7 macrophages.The levels of proteins associated with the nuclear factor-kappa B(NF-κB)pathway were examined by western blotting and immunofluorescence,demonstrating that fleagrass downregulated the expression of TLR4,MyD88,NF-κB/p65,and iNOS and blocked the nuclear translocation of NF-κB/p65.Furthermore,fleagrass exhibited acute anti-inflammatory activity in paw oedema models.The results confirm that fleagrass exhibits remarkable anti-inflammatory activity and can be used in alleviating inflammation,suggesting that fleagrass has the potential to be a novel anti-inflammatory agent. 展开更多
关键词 Fleagrass Anti-inflammatory activities TLR4/MyD88/NF-κB signaling pathway Ethnopharmacology
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Low-temperature Plasma Promotes Fibroblast Proliferation in Wound Healing by ROS-activated NF-κB Signaling Pathway 认领 引用 被引量：6
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作者 Xing-min SHI Gui-min XU +6 位作者 Guan-jun ZHANG Jin-ren LIU Yue-ming WU Ling-ge GAO Yang YANG Zheng-shi CHANG Cong-wei YAO 《Journal of Huazhong University of Science and Technology(Medical Sciences)》 2018年第1期107-114,共8页
Low-temperature plasma(LTP)has shown great promise in wound healing,although the underlying mechanism remains poorly understood.In the present study,an argon atmospheric pressure plasma jet was employed to treat L929 ... Low-temperature plasma(LTP)has shown great promise in wound healing,although the underlying mechanism remains poorly understood.In the present study,an argon atmospheric pressure plasma jet was employed to treat L929 murine fibroblasts cultured in vitro and skin wounds in BALB/c mice.The in vitro analysis revealed that treatment of fibroblasts with LTP for 15 s resulted in a significant increase in cell proliferation,secretion of epidermal growth factor(EGF)and transforming growth factor-β1(TGF-β1),production of intracellular reactive oxygen species(ROS),and the percentage of cells in S phase,protein expression of phosphorylated p65(P-p65)and cyclin D1,but a noted decrease in the protein expression of inhibitor kappa B(IκB).The in vivo experiments demonstrated that 30-s LTP treatment enhanced the number of fibroblasts and the ability of collagen synthesis,while 50-s treatment led to the opposite outcomes.These results suggested that LTP treatment promotes the fibroblast proliferation in wound healing by inducing the generation of ROS,upregulating the expression of P-p65,downregulating the expression of IκB,and activating the NF-κB signaling pathway and consequently altering cell cycle progression(increased DNA synthesis in S phage). 展开更多
关键词 low-temperature plasma fibroblast proliferation NF-κB signaling pathway cell cycle reactive oxygen species
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Downregulation of MUC1 Inhibits Proliferation and Promotes Apoptosis by Inactivating NF-κB Signaling Pathway in Human Nasopharyngeal Carcinoma 认领 引用 被引量：1
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作者 WU Shou-Wu LIN Shao-Kun +11 位作者 NIAN Zhong-Zhu WANG Xin-Wen LIN Wei-Nian ZHUANG Li-Ming WU Zhi-Sheng HUANG Zhi-Wei WANG A-Min GAO Ni-Li CHEN Jia-Wen YUAN Wen-Ting LU Kai-Xian LIAO Jun 《生物化学与生物物理进展》 SCIE CAS CSCD 北大核心 2024年第9期2182-2193,共12页
Objective To investigate the effect of mucin 1(MUC1)on the proliferation and apoptosis of nasopharyngeal carcinoma(NPC)and its regulatory mechanism.Methods The 60 NPC and paired para-cancer normal tissues were collect... Objective To investigate the effect of mucin 1(MUC1)on the proliferation and apoptosis of nasopharyngeal carcinoma(NPC)and its regulatory mechanism.Methods The 60 NPC and paired para-cancer normal tissues were collected from October 2020 to July 2021 in Quanzhou First Hospital.The expression of MUC1 was measured by real-time quantitative PCR(qPCR)in the patients with PNC.The 5-8F and HNE1 cells were transfected with siRNA control(si-control)or siRNA targeting MUC1(si-MUC1).Cell proliferation was analyzed by cell counting kit-8 and colony formation assay,and apoptosis was analyzed by flow cytometry analysis in the 5-8F and HNE1 cells.The qPCR and ELISA were executed to analyze the levels of TNF-αand IL-6.Western blot was performed to measure the expression of MUC1,NFкB and apoptosis-related proteins(Bax and Bcl-2).Results The expression of MUC1 was up-regulated in the NPC tissues,and NPC patients with the high MUC1 expression were inclined to EBV infection,growth and metastasis of NPC.Loss of MUC1 restrained malignant features,including the proliferation and apoptosis,downregulated the expression of p-IкB、p-P65 and Bcl-2 and upregulated the expression of Bax in the NPC cells.Conclusion Downregulation of MUC1 restrained biological characteristics of malignancy,including cell proliferation and apoptosis,by inactivating NF-κB signaling pathway in NPC. 展开更多
关键词 mucin 1 nasopharyngeal carcinoma NF-κB signaling pathway proliferation apoptosis
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Apatinib reduces liver cancer cell multidrug resistance by modulating NF-κB signaling pathway 认领 引用
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作者 XIAOXIAO HE XUEQING ZHOU +4 位作者 JINPENG ZHANG MINGFEI ZHANG DANHONG ZENG HENG ZHANG SHUCAI YANG 《BIOCELL》 SCIE 2024年第9期1331-1341,共11页
Objectives:This investigation aimed to elucidate the inhibitory impact of apatinib on the multidrug resistance of liver cancer both in vivo and in vitro.Methods:To establish a Hep3B/5-Fu resistant cell line,5-Fu conce... Objectives:This investigation aimed to elucidate the inhibitory impact of apatinib on the multidrug resistance of liver cancer both in vivo and in vitro.Methods:To establish a Hep3B/5-Fu resistant cell line,5-Fu concentrations were gradually increased in the culture media.Hep3B/5-Fu cells drug resistance and its alleviation by apatinib were confirmed via flow cytometry and Cell Counting Kit 8(CCK8)test.Further,Nuclear factor kappa B(NF-κB)siRNA was transfected into Hep3B/5-Fu cells to assess alterations in the expression of multidrug resistance(MDR)-related genes and proteins.Nude mice were injected with Hep3B/5-Fu cells to establish subcutaneous xenograft tumors and then categorized into 8 treatment groups.The treatments included oxaliplatin,5-Fu,and apatinib.In the tumor tissues,the expression of MDRrelated genes was elucidated via qRT-PCR,immunohistochemistry,and Western blot analyses.Results:The apatinibtreated mice indicated slower tumor growth with smaller size compared to the control group.Both the in vivo and in vitro investigations revealed that the apatinib-treated groups had reduced expression of MDR genes GST-pi,LRP,MDR1,and p-p65.Conclusions:Apatinib effectively suppresses MDR in human hepatic cancer cells by modulating the expression of genes related to MDR,potentially by suppressing the NF-κB signaling pathway. 展开更多
关键词 Apatinib Liver cancer Multidrug resistance NF-κB signaling pathway
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Kuicolong-yu enema decoction retains traditional Chinese medicine enema attenuates inflammatory response ulcerative colitis through TLR4/NF-κB signaling pathway 认领 引用 被引量：3
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作者 Li Han Kun Tang +3 位作者 Xiao-Li Fang Jing-Xi Xu Xi-Yun Mao Ming Li 《World Journal of Gastrointestinal Surgery》 SCIE 2024年第4期1149-1154,共6页
BACKGROUND Ulcer colitis(UC)is a chronic,nonspecific,and noninfectious inflammatory bowel disease.Recently,Toll-like receptors(TLRs)have been found to be closely associated with clinical inflammatory diseases.Achievin... BACKGROUND Ulcer colitis(UC)is a chronic,nonspecific,and noninfectious inflammatory bowel disease.Recently,Toll-like receptors(TLRs)have been found to be closely associated with clinical inflammatory diseases.Achieving complete remission in patients with intermittent periods of activity followed by dormancy is challenging.Moreover,no study has explored the mechanism by which Kuicolong-yu enema decoction retains traditional Chinese medicine enemas to attenuate the inflammatory response in UC.AIM To explore the mechanism by which Kuicolong-yu enema decoction retains traditional Chinese medicine enemas to attenuate the inflammatory response in UC.METHODS This prospective clinical study included patients who met the exclusion criteria in 2020 and 2021.The patients with UC were divided into two groups(control and experimental).The peripheral blood of the experimental and control groups were collected under aseptic conditions.The expression of TLR4 protein,NF-κB,IL-6,and IL-17 was detected in the peripheral blood of patients in the experimental group and control group before and 1 month after taking the drug.Linear co rrelation analysis was used to analyze the relationship between the expression level of TLR4 protein and the expression levels of downstream signal NF-κB and inflammatory factors IL-6 and IL-17,and P<0.05 was considered statistically significant.RESULTS There were no significant differences in the patient characteristics between the control and experimental groups.The results showed that the expression levels of TLR4 and NF-κB in the experimental group were significantly lower than those in the control group(P<0.05).The levels of IL-6 and IL-17 in the experimental group were significantly lower than those in the control group(P<0.05).The TLR4 protein expression in the experimental group was positively correlated with the expression level of downstream signal NF-κB and was positively correlated with the levels of downstream inflammatory cytokines IL-6 and IL-17(r=0.823,P<0.05).CONCLUSION Kuicolong-yu enema decoction retains traditional Chinese medicine enema attenuates the inflammatory response of UC through the TLR4/NF-κB signaling pathway. 展开更多
关键词 Ulcerative colitis TLR4 NF-κB signaling pathway Kuicolong-yu enema
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Taurolidine improved protection against highly pathogenetic avian influenza H5N1 virus lethal-infection in mouse model by regulating the NF-κB signaling pathway 认领 引用 被引量：1
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作者 Chaoxiang Lv Yuanguo Li +15 位作者 Tiecheng Wang Qiqi Zhang Jing Qi Mingwei Sima Entao Li Tian Qin Zhuangzhuang Shi Fangxu Li Xuefeng Wang Weiyang Sun Na Feng Songtao Yang Xianzhu Xia Ningyi Jin Yifa Zhou Yuwei Gao 《Virologica Sinica》 SCIE CAS CSCD 2023年第1期119-127,共9页
Taurolidine(TRD),a derivative of taurine,has anti-bacterial and anti-tumor effects by chemically reacting with cell-walls,endotoxins and exotoxins to inhibit the adhesion of microorganisms.However,its application in a... Taurolidine(TRD),a derivative of taurine,has anti-bacterial and anti-tumor effects by chemically reacting with cell-walls,endotoxins and exotoxins to inhibit the adhesion of microorganisms.However,its application in antiviral therapy is seldom reported.Here,we reported that TRD significantly inhibited the replication of influenza virus H5N1 in MDCK cells with the half-maximal inhibitory concentration(EC50)of 34.45μg/mL.Furthermore,the drug inhibited the amplification of the cytokine storm effect and improved the survival rate of mice lethal challenged with H5N1(protection rate was 86%).Moreover,TRD attenuated virus-induced lung damage and reduced virus titers in mice lungs.Administration of TRD reduced the number of neutrophils and increased the number of lymphocytes in the blood of H5N1 virus-infected mice.Importantly,the drug regulated the NF-κB signaling pathway by inhibiting the separation of NF-κB and IκBa,thereby reducing the expression of inflammatory factors.In conclusion,our findings suggested that TRD could act as a potential anti-influenza drug candidate in further clinical studies. 展开更多
关键词 Influenza viruses H5N1 Taurolidine(TRD) Cytokine storms Inflammatory response NF-κB signaling pathway
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Novel phenanthrene/bibenzyl trimers from the tubers of Bletilla striata attenuate neuroinflammation via inhibition of NF-κB signaling pathway 认领 引用 被引量：1
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作者 SHAO Siyuan SUN Mohan +5 位作者 MA Xianjie JIANG Jianwei TIAN Jinying ZHANG Jianjun YE Fei LI Shuai 《Chinese Journal of Natural Medicines》 SCIE CAS CSCD 2024年第5期441-454,共14页
Five novel(9,10-dihydro)phenanthrene and bibenzyl trimers,as well as two previously identified biphenanthrenes and bibenzyls,were isolated from the tubers of Bletilla striata.Their structures were elucidated through c... Five novel(9,10-dihydro)phenanthrene and bibenzyl trimers,as well as two previously identified biphenanthrenes and bibenzyls,were isolated from the tubers of Bletilla striata.Their structures were elucidated through comprehensive analyses of NMR and HRESIMS spectroscopic data.The absolute configurations of these compounds were determined by calculating rotational energy barriers and comparison of experimental and calculated ECD curves.Compounds 5b and 6 exhibited inhibitory effects on LPS-induced NO production in BV-2 cells,with IC50 values of 12.59±0.40 and 15.59±0.83μmol·L-1,respectively.A mechanistic study suggested that these compounds may attenuate neuroinflammation by reducing the activation of the AKT/IκB/NF-κB signaling pathway.Additionally,compounds 3a,6,and 7 demonstrated significant PTP1B inhibitory activities,with IC50 values of 1.52±0.34,1.39±0.11,and 1.78±0.01μmol·L-1,respectively.Further investigation revealed that compound 3a might inhibit LPS-induced PTP1B overexpression and NF-κB activation,thereby mitigating the neuroinflammatory response in BV-2 cells. 展开更多
关键词 Bletilla striata Phenanthrene/bibenzyl trimer NO inhibition AKT/IκB/NF-κB signaling pathway PTP1B inhibitory effect
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β-arrestin 2 attenuates lipopolysaccharide-induced liver injury via inhibition of TLR4/NF-κB signaling pathwaymediated inflammation in mice 认领 引用 被引量：13
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作者 Meng-Ping Jiang Chun Xu +6 位作者 Yun-Wei Guo Qian-Jiang Luo Lin Li Hui-Ling Liu Jie Jiang Hui-Xin Chen Xiu-Qing Wei 《World Journal of Gastroenterology》 SCIE CAS 2018年第2期216-225,共10页
AIM To study the role and the possible mechanism of β-arrestin 2 in lipopolysaccharide(LPS)-induced liver injury in vivo and in vitro.METHODS Male β-arrestin 2+/+ and β-arrestin 2-/-C57 BL/6 J mice were used ... AIM To study the role and the possible mechanism of β-arrestin 2 in lipopolysaccharide(LPS)-induced liver injury in vivo and in vitro.METHODS Male β-arrestin 2+/+ and β-arrestin 2-/-C57 BL/6 J mice were used for in vivo experiments, and the mouse macrophage cell line RAW264.7 was used for in vitro experiments. The animal model was established via intraperitoneal injection of LPS or physiological sodium chloride solution. Blood samples and liver tissues were collected to analyze liver injury and levels of pro-inflammatory cytokines. Cultured cell extracts were collected to analyze the production of pro-inflammatory cytokines and expression of key molecules involved in the TLR4/NF-κB signaling pathway.RESULTS Compared with wild-type mice, the β-arrestin 2 knockout mice displayed more severe LPS-induced liver injury and significantly higher levels of proinflammatory cytokines, including interleukin(IL)-1β, IL-6, tumor necrosis factor(TNF)-α, and IL-10. Compared with the control group, pro-inflammatory cytokines(including IL-1β, IL-6, TNF-α, and IL-10) produced by RAW264.7 cells in the β-arrestin 2 si RNA group were significantly increased at 6 h after treatment with LPS. Further, key molecules involved in the TLR4/NF-κB signaling pathway, including phosphoIκBα and phosho-p65, were upregulated.CONCLUSION β-arrestin 2 can protect liver tissue from LPS-induced injury via inhibition of TLR4/NF-κB signaling pathwaymediated inflammation. 展开更多
关键词 Lipopolysaccharide Liver injury β-arrestin 2 TLR4/NF-κB signaling pathway Pro-inflammatory cytokines
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Recombinant adeno-associated virus serotype 9 with p65 ribozyme protects H9c2 cells from oxidative stress through inhibiting NF-κB signaling pathway 认领 引用 被引量：6
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作者 Zhan SUN Yi-Tong MA +1 位作者 Bang-Dang CHEN Fen LIU 《Journal of Geriatric Cardiology》 SCIE CAS CSCD 2014年第4期311-315,共5页
Background Oxidative stress is a major mechanism underlying the pathogenesis of cardiovascular disease. It can trigger inflammatory cascades which are primarily mediated via nuclear factor-κB （NF-κB）. The NF-κB t... Background Oxidative stress is a major mechanism underlying the pathogenesis of cardiovascular disease. It can trigger inflammatory cascades which are primarily mediated via nuclear factor-κB （NF-κB）. The NF-κB transcription factor family includes several subunits （p50, p52, p65, c-Rel, and Rel B） that respond to myocardial ischemia. It has been proved that persistent myocyte NF-κB p65 activation in heart failure exacerbates cardiac remodeling. Mechods A recombinant adeno-associated virus serotype 9 carrying enhanced green fluorescent protein and anti-NF-κB p65 ribozyme （AAV9-R65-CMV-eGFP） was constructed. The cells were assessed by MTT assay, Annexin V–propidium iodide dual staining to study apoptosis. The expression of P65 and P50 were assessed by Western blot to investigate the under-lying molecular mechanisms. Results After stimulation with H2O2 for 6 h, H9c2 cells viability decreased significantly, a large fraction of cells underwent apoptosis. We observed a rescue of H9c2 cells from H2O2-induced apoptosis in pretreatment with AAV9-R65-CMV-eGFP. Moreover, AAV9-R65-CMV-eGFP decreased H2O2-induced P65 expression. Conclusions AAV9-R65-CMV-eGFP protects H9c2 cells from oxidative stress induced apoptosis through down-regulation of P65 expression. These observations indicate that AAV9-R65-CMV-eGFP has the potential to exert cardioprotective effects against oxidative stress, which might be of great importance to clinical efficacy for cardiovascular disease. 展开更多
关键词 Cardiomyocytes Adenovirus R65 ribozyme Apoptosis NF-κB pathway
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Phycocyanin attenuates X-ray-induced pulmonary inflammation via the TLR2-MyD88-NF-κB signaling pathway 认领 引用 被引量：2
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作者 LIU Qi LI Wenjun +3 位作者 LU Lina LIU Bin DU Zhenning QIN Song 《Journal of Oceanology and Limnology》 SCIE CAS CSCD 2019年第5期1678-1685,共8页
Phycocyanin (PC), a natural algal protein, is reported for having anti-oxidant and antiinfl ammatory properties. We investigated its ability to attenuate lung infl ammation in mice subjected to X-ray radiation. Male C... Phycocyanin (PC), a natural algal protein, is reported for having anti-oxidant and antiinfl ammatory properties. We investigated its ability to attenuate lung infl ammation in mice subjected to X-ray radiation. Male C57BL/6 mice were assigned to the control, total body irradiation, PC pretreatment, and PC treatment groups. Mice in the PC pretreatment group were gavaged with 200 mg/kg PC for 7 consecutive days before irradiation, and those in the PC treatment group were gavaged with 200 mg/kg PC for 7 consecutive days after irradiation. Lungs were collected on Day 7 after irradiation exposure. Hematoxylin and eosin staining of mouse lung sections showed considerable infl ammation damage 7 days after irradiation compared with the control lung but a reduction in pathological injury in the PC treatment group. Pretreatment or treatment with PC signifi cantly decreased levels of interleukin-6 and tumor necrosis factor-α in the lung, and also increased the relative mRNA expression of superoxide dismutase and glutathione. In vivo, PC signifi cantly reduced the expression of Toll-like receptor TLR2, myeloid diff erentiation primary response Myd88, and nuclear factor NF-κB, at both the transcriptional and translation level. Taken together, these data indicated that PC attenuated lung infl ammatory damage induced by radiation by blocking the TLR2- MyD88-NF-κB signaling pathway. Therefore, PC could be a protective agent against radiation-induced infl ammatory damage in normal tissues. 展开更多
关键词 phycocyanin infl ammatory TLR2-MyD88-NF-κB signaling pathway
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Calcitriol attenuates liver fibrosis through hepatitis C virus nonstructural protein 3-transactivated protein 1-mediated TGF β1/Smad3 and NF-κB signaling pathways 认领 引用 被引量：1
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作者 Liu Shi Li Zhou +13 位作者 Ming Han Yu Zhang Yang Zhang Xiao-Xue Yuan Hong-Ping Lu Yun Wang Xue-Liang Yang Chen Liu Jun Wang Pu Liang Shun-Ai Liu Xiao-Jing Liu Jun Cheng Shu-Mei Lin 《World Journal of Gastroenterology》 SCIE CAS 2023年第18期2798-2817,共20页
BACKGROUND Hepatic fibrosis is a serious condition,and the development of hepatic fibrosis can lead to a series of complications.However,the pathogenesis of hepatic fibrosis remains unclear,and effective therapy optio... BACKGROUND Hepatic fibrosis is a serious condition,and the development of hepatic fibrosis can lead to a series of complications.However,the pathogenesis of hepatic fibrosis remains unclear,and effective therapy options are still lacking.Our group identified hepatitis C virus nonstructural protein 3-transactivated protein 1(NS3TP1) by suppressive subtractive hybridization and bioinformatics analysis,but its role in diseases including hepatic fibrosis remains undefined.Therefore,additional studies on the function of NS3TP1 in hepatic fibrosis are urgently needed to provide new targets for treatment.AIM To elucidate the mechanism of NS3TP1 in hepatic fibrosis and the regulatory effects of calcitriol on NS3TP1.METHODS Twenty-four male C57BL/6 mice were randomized and separated into three groups,comprising the normal,fibrosis,and calcitriol treatment groups,and liver fibrosis was modeled by carbon tetrachloride(CCl4).To evaluate the level of hepatic fibrosis in every group,serological and pathological examinations of the liver were conducted.TGF-β1 was administered to boost the in vitro cultivation of LX-2 cells.NS3TP1,α-smooth muscle actin(α-SMA),collagen I,and collagen Ⅲ in every group were examined using a Western blot and real-time quantitative polymerase chain reaction.The activity of the transforming growth factor beta 1(TGFβ1)/Smad3 and NF-κB signaling pathways in each group of cells transfected with pcDNA-NS3TP1 or siRNA-NS3TP1 was detected.The statistical analysis of the data was performed using the Student’s t test.RESULTS NS3TP1 promoted the activation,proliferation,and differentiation of hepatic stellate cells(HSCs)and enhanced hepatic fibrosis via the TGFβ1/Smad3 and NF-κB signaling pathways,as evidenced by the presence of α-SMA,collagen I,collagen Ⅲ,p-smad3,and p-p65 in LX-2 cells,which were upregulated after NS3TP1 overexpression and downregulated after NS3TP1 interference.The proliferation of HSCs was lowered after NS3TP1 interference and elevated after NS3TP1 overexpression,as shown by the luciferase assay.NS3TP1 inhibited the apoptosis of HSCs.Moreover,both Smad3 and p65 could bind to NS3TP1,and p65 increased the promoter activity of NS3TP1,while NS3TP1 increased the promoter activity of TGFβ1 receptor I,as indicated by coimmunoprecipitation and luciferase assay results.Both in vivo and in vitro,treatment with calcitriol dramatically reduced the expression of NS3TP1.Calcitriol therapy-controlled HSCs activation,proliferation,and differentiation and substantially suppressed CCl4-induced hepatic fibrosis in mice.Furthermore,calcitriol modulated the activities of the above signaling pathways via downregulation of NS3TP1.CONCLUSION Our results suggest that calcitriol may be employed as an adjuvant therapy for hepatic fibrosis and that NS3TP1 is a unique,prospective therapeutic target in hepatic fibrosis. 展开更多
关键词 Nonstructural protein 3-transactivated protein 1 Calcitriol Liver fibrosis Hepatic stellate cells Mouse model TGFβ1/Smad3 NF-κB Signaling pathway
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The Effect of Semen Ziziphi Spinosae Extract on the p38MAPK/NF-κB Signaling Pathway in Insomniac Rats 认领 引用 被引量：1
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作者 Mingyu Ji Wei Xiong +4 位作者 Zijing Xu Peipei Zhang Shuyu Li Qian Wang Dexian Jia 《Chinese Medicine and Natural Products》 CAS 2024年第4期145-152,共8页
Objective The objective of the study was to explore whether Suanzaoren(Semen Ziziphi Spinosae,SZS)extract could improve insomnia by inhibiting the p38 mitogenactivated protein kinase(p38MAPK)uclear factor-κB(NF-κB)s... Objective The objective of the study was to explore whether Suanzaoren(Semen Ziziphi Spinosae,SZS)extract could improve insomnia by inhibiting the p38 mitogenactivated protein kinase(p38MAPK)uclear factor-κB(NF-κB)signaling pathway.Methods Forty SPF-grade Sprague-Dawley(SD)rats were included in the study,with 10 randomly selected rats serving as the control group.The remaining rats were injected intraperitoneally with p-chlorophenylalanine(PCPA)for 6 days to establish an insomnia model.After successful modeling,the rats were divided into the model group,SZS extract group(3.0 g/kg),and zopiclone group(1.25 g/kg).The rats in the SZS extract and zopiclone groups were administered with the corresponding drugs via gavage for 7 days,while the rats in the control and model groups received distilled water.Sleep latency and sleep duration were recorded,and behavioral changes were observed through elevated plusmaze and open field tests.The levels of oxidative stress markers and serum inflammatory factors were measured by enzyme-linked immunosorbent assay(ELISA).The expression levels of p38 MAPK,p-p38MAPK,p-NF-κBp65,and NF-κBp65 protein in the cerebral cortex were detected by Western blot.Neuronal structures in the cerebral cortex were observed under a transmission electron microscope.Results Compared with the control group,the model group exhibited abnormal appearances,significant body mass loss(p<0.001),prolonged sleep latency and shortened sleep duration(p<0.001).The SZS extract and zopiclone groups showed significant improvements in these parameters compared with the model group.Compared with the control group,the model group showed significant reduction in total movement distance(p<0.001),fewer entries into the central zone(p<0.01),and significant decrease in rearing frequency(p<0.001);the levels of glutathione peroxidase(GSH-Px)and catalase(CAT)in the hippocampus were significantly reduced(p<0.001);the serum levels of interleukin-1β(IL-1β),tumor necrosis factor-α(TNF-α),and the expression levels of p-p38MAPK and p-NF-κBp65 in the cerebral cortex were significantly increased(p<0.05).Compared with the model group,the SZS extract group showed significant increase in movement distance(p<0.01)and rearing frequency(p<0.001),significantly increased the GSH-Px and CAT levels(p<0.001),and decreased the IL-1βand TNF-αlevels(p<0.01);furthermore,the SZS extract group showed a significantly reduced p-p38MAPK and p-NF-κBp65 levels(p<0.05).The SZS extract group showed significant improvement in the neuronal structure compared with the model group.Conclusion SZS extract can inhibit the p38MAPK/NF-κB signaling pathway to improve insomnia. 展开更多
关键词 Semen Ziziphi Spinosae extract p38MAPK/NF-κB signaling pathway insomnia oxidative stress inflammatory factors
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