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Trans-spinal magnetic stimulation upregulates microglial SOCS3 to attenuate neuroinflammation in chronic constriction injury-induced neuropathic pain 认领 引用
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作者 Qi Wu Xingjun Xu +10 位作者 Chenyuan Zhai Jili Cai Zun Wang Lu Fang Yu Wang Yilun Qian Manyu Dong Liang Hu Tong Wang Ying Shen Wentao Liu 《Neural Regeneration Research》 SCIE CAS CSCD 2026年第7期3092-3102,共11页
Current treatments for neuropathic pain are suboptimal,necessitating the search for more effective therapeutics.Our previous study showed that inhibition of neuroinflammation in the spinal cord induced analgesic effec... Current treatments for neuropathic pain are suboptimal,necessitating the search for more effective therapeutics.Our previous study showed that inhibition of neuroinflammation in the spinal cord induced analgesic effects,and focal repetitive trans-spinal magnetic stimulation showed an anti-neuroinflammatory effect in spinal cord injury rat models.Here,we speculated that repetitive trans-spinal magnetic stimulation might induce an anti-inflammatory effect to alleviate neuropathic pain by upregulating calmodulin-dependent protein kinase kinase beta(CaMKKβ)/adenosine 5′-monophosphate-activated protein kinase(AMPK)/suppressor of cytokine signaling-3(SOCS3)signaling in microglia.Experiments have found that non-invasive focal repetitive trans-spinal magnetic stimulation effectively alleviates mechanical allodynia and spinal neuroinflammation in rats with neuropathic pain induced by chronic sciatic nerve ligation.Further research found that repetitive trans-spinal magnetic stimulation upregulated the expression of SOCS3 in spinal microglia,which subsequently inhibited the phosphorylation of p38 mitogen-activated protein kinase and signal transducer and activator of transcription 3 and nuclear factor-kappa B p65 nuclear translocation in rats with neuropathic pain,thereby suppressing neuroinflammation.The upregulation of SOCS3 by repetitive trans-spinal magnetic stimulation may be achieved through the activation of the CaMKKβ/AMPK signaling pathway in microglia.The results suggested that focal repetitive trans-spinal magnetic stimulation inhibits spinal neuroinflammation and alleviates neuropathic pain by activating the CaMKKβ/AMPK/SOCS3 signaling pathway in spinal microglia.This mechanism provides an effective noninvasive treatment for neuropathic pain caused by peripheral nerve injury. 展开更多
关键词 CaMKKβ/AMPK/SOCS3 signaling chronic constriction injury mechanical pain sensitivity microglia neuropathic pain neuroinflammation nuclear factor-κB p65 repetitive trans-spinal magnetic stimulation STAT3
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利多卡因通过激活AMPK/SOCS3信号通路改善阿霉素引起的急性心肌损伤 认领 引用 被引量：2
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作者 陈建溯 宋雅君 +4 位作者 吴胜兰 周超一 金莱 刘文涛 李庆国 《南京医科大学学报（自然科学版）》 CAS 北大核心 2023年第8期1068-1075,共8页
目的:研究利多卡因(lidocaine,Lido)对阿霉素(doxorubicin,Dox)引起小鼠心脏损伤的治疗效果及作用机制。方法:32只SPF小鼠随机分为Saline组、Dox组、Dox+Lido组、Lido组4组(n=8),观察并检测各组小鼠体重、生存率、多普勒血流成像、心电... 目的:研究利多卡因(lidocaine,Lido)对阿霉素(doxorubicin,Dox)引起小鼠心脏损伤的治疗效果及作用机制。方法:32只SPF小鼠随机分为Saline组、Dox组、Dox+Lido组、Lido组4组(n=8),观察并检测各组小鼠体重、生存率、多普勒血流成像、心电图、心脏超声,以及血浆肌酸激酶同工酶(creatine kinase-MB,CK-MB)、肌钙蛋白I(cardiac troponin I,cTnI),心肌组织中组织因子(tissue factor,TF)、基质金属蛋白酶9(matrix metalloprotein 9,MMP-9)、磷酸化磷酸腺苷活化蛋白激酶(phosphorylated adenosine 5’-monophosphate-activated protein kinase,p-AMPK)、缝隙连接蛋白(connexin43,Cx43)、细胞因子信号转导抑制因子3(recombinant suppressors of cytokine signaling 3,SOCS3)的含量。结果:与Saline组比较,Dox组小鼠体重、生存率明显降低,心率降低、QRS波时限及QT间期延长,血浆CK-MB、cTnI值明显上升,心脏挛缩,心腔变小,TF、MMP-9升高,心脏组织中p-AMPK、SOCS3、Cx43表达减低;与Dox组相比,Dox+Lido组小鼠体重、生存率增加,心率上升,QRS波时限及QT间期正常,血浆CK-MB、cTnI值处于正常区间,心脏大小未见明显改变,TF、MMP-9降低,心脏组织中p-AMPK、SOCS3、Cx43表达增加。结论:利多卡因能通过激活p-AMPK/SOCS3/Cx43信号通路和抑制TF/MMP-9高表达改善阿霉素诱导的急性心肌损伤。 展开更多
关键词 阿霉素 心肌损伤 利多卡因 AMPK CX43 SOCS3
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CaMKKβ通过激活AMPK/JAK2/STAT3信号促进小鼠单核巨噬细胞向M2表型转换 认领 引用 被引量：7
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作者 孔祥歆 刘卉芳 陈凤玲 《上海交通大学学报（医学版）》 CAS CSCD 北大核心 2017年第7期914-923,共10页
目的·探明钙离子/钙调蛋白依赖性蛋白激酶激酶β(CaMKKβ)在白介素4(IL-4)诱导的RAW264.7细胞极化过程中的作用和机制。方法·RT-PCR和ELISA检测IL-4诱导RAW264.7细胞极化水平,Western blotting测定极化过程中CaMKKβ、AMPK、J... 目的·探明钙离子/钙调蛋白依赖性蛋白激酶激酶β(CaMKKβ)在白介素4(IL-4)诱导的RAW264.7细胞极化过程中的作用和机制。方法·RT-PCR和ELISA检测IL-4诱导RAW264.7细胞极化水平,Western blotting测定极化过程中CaMKKβ、AMPK、JAK2、STAT3蛋白表达及磷酸化水平。慢病毒为载体的shRNA稳定干扰RAW264.7细胞CaMKKβ表达,RT-PCR和ELISA检测IL-4诱导下细胞极化水平的改变,Western blotting检测AMPK、JAK2、STAT3蛋白及磷酸化蛋白的表达。分别特异性阻断AMPK、JAK2和STAT3蛋白活性,经RT-PCR检测IL-4诱导下RAW264.7细胞极化水平的改变。结果·IL-4主要诱导RAW264.7细胞向M2型巨噬细胞极化(P<0.05),且CaMKKβ、AMPK、JAK2、STAT3的磷酸化水平明显升高(均P<0.05)。shRNA稳定干扰RAW264.7细胞CaMKKβ表达后,IL-4促进巨噬细胞向M2型极化作用降低(P<0.05),且AMPK、JAK2和STAT3的磷酸化水平降低(均P<0.05)。分别阻断AMPK、JAK2和STAT3,巨噬细胞向M2型极化减少(均P<0.05)。结论·CaMKKβ通过激活AMPK/JAK2/STAT3信号通路,促进IL-4诱导的巨噬细胞M2型极化。 展开更多
关键词 CaMKKβ AMPK JAK2 STAT3 巨噬细胞极化
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miR-145-3p通过调控CaMkkβ/AMPK/CREB通路对MPP+诱导PD细胞模型线粒体自噬的影响 认领 引用 被引量：3
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作者 文晓东 罗宁 +4 位作者 周欣梅 卢建政 曾振 张艺 王春玲 《安徽医科大学学报》 CAS 北大核心 2023年第11期1846-1853,共8页
目的探讨miR-145-3p对1-甲基-4苯基吡啶离子(MPP+)诱导的帕金森病(PD)细胞模型线粒体自噬的影响及其机制。方法将人神经母细胞瘤细胞(SH-SY5Y)分为对照组、模型组、模拟物(mimics)组、钙调蛋白依赖性蛋白激酶激酶β(CaMkkβ)抑制剂(S... 目的探讨miR-145-3p对1-甲基-4苯基吡啶离子(MPP+)诱导的帕金森病(PD)细胞模型线粒体自噬的影响及其机制。方法将人神经母细胞瘤细胞(SH-SY5Y)分为对照组、模型组、模拟物(mimics)组、钙调蛋白依赖性蛋白激酶激酶β(CaMkkβ)抑制剂(STO-609)组、mimics+STO-609组、环磷酸腺苷反应元件结合蛋白(CREB)抑制剂(KG-501)组、mimics+KG-501组和STO-609+KG-501组。流式细胞术检测细胞凋亡,透射电镜观察自噬体结构,Western blot检测凋亡、自噬和CaMkkβ/腺苷酸活化蛋白激酶(AMPK)/CREB通路相关蛋白的表达。结果与对照组相比,模型组细胞凋亡率、Bcl-2关联X蛋白(Bax)、半胱氨酸蛋白酶-3(Caspase-3)和微管相关蛋白轻链3-I(LC3-Ⅰ)蛋白表达水平均升高(P<0.01),自噬体结构减少,B淋巴细胞瘤-2(Bcl-2)、自噬基因(Beclin-1)、微管相关蛋白轻链3-II(LC3-Ⅱ)、磷酸化钙调蛋白依赖性蛋白激酶激酶β(p-CaMkkβ)、磷酸化腺苷酸活化蛋白激酶(p-AMPK)、磷酸化环磷酸腺苷反应元件结合蛋白(p-CREB)蛋白水平均降低(P<0.01);与模型组相比,mimics组细胞凋亡率、Bax、Caspase-3和LC3-Ⅰ蛋白表达水平降低(P<0.05),自噬体结构增多,Bcl-2、Beclin-1、LC3-Ⅱ、p-CaMkkβ、p-AMPK、p-CREB蛋白水平升高(P<0.05),STO-609组和KG-501组趋势相同均与mimics组相反;与mimics组相比,mimics+STO-609组和mimics+KG-501组细胞凋亡率、Bax、Caspase-3和LC3-Ⅰ蛋白表达水平升高(P<0.01),自噬体结构减少,Bcl-2、Beclin-1、LC3-Ⅱ、p-CaMkkβ、p-AMPK、p-CREB蛋白水平降低(P<0.01);与STO-609组相比,STO-609+KG-501组细胞凋亡率、Bax、Caspase-3和LC3-Ⅰ蛋白表达水平升高(P<0.01),自噬体结构减少,Bcl-2、Beclin-1、LC3-Ⅱ、p-CaMkkβ、p-AMPK、p-CREB蛋白水平降低(P<0.05)。结论miR-145-3p能够抑制MPP+诱导的PD细胞模型的凋亡,促进线粒体自噬,其机制可能与促进CaMkkβ/AMPK/CREB通路的激活有关。 展开更多
关键词 miR-145-3p CaMkkβ/AMPK/CREB通路 帕金森病 线粒体自噬 细胞凋亡
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Hepatic TRPC3 loss contributes to chronic alcohol consumption-induced hepatic steatosis and liver injury in mice 认领 引用
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作者 Qinchao Ding Rui Guo +13 位作者 Liuyi Hao Qing Song Ai Fu Shanglei Lai Tiantian Xu Hui Zhuge Kaixin Chang Yanli Chen Haibin Wei Daxi Ren Zhaoli Sun Zhenyuan Song Xiaobing Dou Songtao Li 《Life Metabolism》 2024年第1期51-66,共16页
Emerging evidence discloses the involvement of calcium channel protein in the pathological process of liver diseases.Transient receptor potential cation channel subfamily C member 3(TRPC3),a ubiquitously expressed non... Emerging evidence discloses the involvement of calcium channel protein in the pathological process of liver diseases.Transient receptor potential cation channel subfamily C member 3(TRPC3),a ubiquitously expressed non-selective cation channel protein,controls proliferation,inflammation,and immune response via operating calcium influx in various organs.However,our understanding on the biofunction of hepatic TRPC3 is still limited.The present study aims to clarify the role and potential mechanism(s)of TRPC3 in alcohol-associated liver disease(ALD).We recently found that TRPC3 expression plays an important role in the disease process of ALD.Alcohol exposure led to a significant reduction of hepatic TRPC3 in patients with alcohol-related hepatitis(AH)and ALD models.Antioxidants(N-acetylcysteine and mitoquinone)intervention improved alcohol-induced suppression of TRPC3 via a miR-339-5p-involved mechanism.TRPC3 loss robustly aggravated the alcohol-induced hepatic steatosis and liver injury in mouse liver;this was associated with the suppression of Ca2+/calmodulin-dependent protein kinase kinase 2(CAMKK2)/AMP-activated protein kinase(AMPK)and dysregulation of genes related to lipid metabolism.TRPC3 loss also enhanced hepatic inflammation and early fibrosis-like change in mice.Replenishing hepatic TRPC3 effectively reversed chronic alcohol-induced detrimental alterations in ALD mice.Briefly,chronic alcohol exposure-induced TRPC3 reduction contributes to the pathological development of ALD via suppression of the CAMKK2/AMPK pathway.Oxidative stress-stimulated miR-339-5p upregulation contributes to alcohol-reduced TRPC3.TRPC3 is the requisite and a potential target to defend alcohol consumption-caused ALD. 展开更多
关键词 TRPC3 alcohol-associated liver disease miR-339-5p hepatic steatosis liver injury CAMKK2/AMPK
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