| 引用本文: | 陶振云,江祖泰,李丽珍,王兰兰,钟炜昕,李粮辉,刘俊乐,陈文华.PKC-ERK1/2通路在臭氧预处理减轻大鼠肝缺血再灌注损伤的作用[J].中国现代应用药学,2021,38(12):1436-1440. |
| TAO Zhenyun,JIANG Zutai,LI Lizhen,WANG Lanlan,ZHONG Weixin,LI Lianghui,LIU Junle,CHEN Wenhua.Effects of PKC-ERK1/2 Pathway on O3 Oxidative Pretreatment to Reduce Hepatic Ischemia Reperfusion Injury in Rats[J].Chin J Mod Appl Pharm(中国现代应用药学),2021,38(12):1436-1440. |
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| PKC-ERK1/2通路在臭氧预处理减轻大鼠肝缺血再灌注损伤的作用 |
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陶振云1, 江祖泰2, 李丽珍3, 王兰兰4, 钟炜昕5, 李粮辉6, 刘俊乐7, 陈文华7
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1.义乌市中心医院, 浙江 义乌 322000;2.福州市第二医院, 福州 350007;3.福建省人民医院, 福州 350001;4.福建省肿瘤医院, 福州 350001;5.福建医科大学附属孟超医院, 福州 350025;6.福建省立医院南院, 福州 350028;7.福建医科大学附属协和医院, 福州 350001
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| 摘要: |
| 目的 探讨PKC介导的ERK1/2信号通路在臭氧（ozone，O3）预处理大鼠肝缺血再灌注中的作用。方法 60只大鼠随机分成6组：对照组、缺血再灌注组、O3预处理组、O3预处理+ERK抑制剂组（O3+PD98059组）、O3预处理+PKC抑制剂组（O3+CHE组）、缺血再灌注+PKC激活剂组（IR+PMA组）。除对照组外，其余各组均进行肝缺血再灌注手术。O3相关组予O3预处理，调节剂组予相应的调节剂。分别检测各组的血清中丙氨酸氨基转移酶、天冬氨酸氨基转氨酶水平，进行病理学观察，Western blotting检测肝组织中的热休克蛋白70（heat shock protein 70，HSP70）、蛋白激酶C（protein kinase C，PKC）和细胞外调节蛋白激酶1/2（extracellular regulated protein kinases，ERK1/2）的表达水平。结果 与对照组相比，缺血再灌注组肝组织细胞损伤明显加重（P<0.05），肝组织中PKC、ERK1/2的磷酸化和HSP70的表达水平明显升高（P<0.05）。与缺血再灌注组相比，O3相关组肝组织细胞损伤明显减轻（P<0.05），肝组织中PKC、ERK1/2的磷酸化和HSP70的表达水平明显升高（P<0.05）。与O3预处理组相比，当使用PKC和ERK1/2抑制剂后，肝组织细胞损伤明显加重（P<0.05），肝组织中PKC、ERK1/2的磷酸化和HSP70的表达水平明显降低（P<0.05）。结论 O3氧化预处理可通过激活PKC介导的ERK1/2信号通路，使HSP70的表达水平明显增加，使大鼠肝脏缺血再灌注损伤明显减轻。 |
| 关键词: 细胞外调节蛋白激酶1/2|热休克蛋白70|蛋白激酶C|臭氧|缺血再灌注 |
| DOI：10.13748/j.cnki.issn1007-7693.2021.12.005 |
| 分类号:R965.1 |
| 基金项目:福建省自然科学基金项目（2016J01543） |
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| Effects of PKC-ERK1/2 Pathway on O3 Oxidative Pretreatment to Reduce Hepatic Ischemia Reperfusion Injury in Rats |
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TAO Zhenyun1, JIANG Zutai2, LI Lizhen3, WANG Lanlan4, ZHONG Weixin5, LI Lianghui6, LIU Junle7, CHEN Wenhua7
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1.Yiwu Central Hospital, Yiwu 322000, China;2.Fuzhou Second Hospital, Fuzhou 350007, China;3.Fujian Provincial People's Hospital, Fuzhou 350001, China;4.Fujian Cancer Hospital, Fuzhou 350001, China;5.Fujian Medical University Mengchao Hospital, Fuzhou 350025, China;6.South Hospital of Fujian Provincial Hospital, Fuzhou 350028, China;7.Fujian Medical University Union Hospital, Fuzhou 350001, China
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| Abstract: |
| OBJECTIVE To explore the role of PKC-mediated ERK1/2 signaling pathway in ozone(O3)preconditioning rat liver ischemia-reperfusion. METHODS Sixty rats were randomly divided into 6 groups:control group, ischemia reperfusion group, O3 pretreatment group, O3 pretreatment+ERK inhibitor group(O3+PD98059 group), O3 pretreatment+PKC inhibitor group(O3+CHE group), ischemia reperfusion+PKC activator group(IR+PMA group). Except for control group, all other groups underwent liver ischemia reperfusion surgery. The O3-related group was pretreated with O3, and the regulator group was given the corresponding regulator. The levels of alanine aminotransferase and aspartate aminotransferase in serum of each group were detected respectively, and pathological observation was performed. Western blotting was used to detect heat shock protein 70(HSP70), protein kinase C(PKC) and extracellular regulated protein kinase 1/2(ERK1/2) expression levels in liver tissue. RESULTS Compared with the control group, ischemia reperfusion group had significantly increased liver tissue cell damage(P<0.05), and the PKC and ERK1/2 phosphorylation and HSP70 expression levels in the liver tissue were significantly increased(P<0.05). Compared with the ischemia reperfusion group, the liver tissue cells of the O3-related group were significantly reduced(P<0.05), the phosphorylation of PKC and ERK1/2 and the expression level of HSP70 in the liver tissue were significantly increased(P<0.05). Compared with the O3 pretreatment group, when PKC and ERK1/2 inhibitors were used, liver tissue cell damage was significantly increased(P<0.05), PKC and ERK1/2 phosphorylation and HSP70 expression levels in liver tissue were significantly reduced(P<0.05). CONCLUSION O3 oxidative pretreatment can significantly increase the expression level of HSP70 by activating the PKC-mediated ERK1/2 signaling pathway, and significantly reduce the liver ischemia-reperfusion injury in rats. |
| Key words: extracellular regulated protein kinases(ERK1/2)|heat shock protein 70(HSP70)|protein kinase C(PKC)|ozone(O3)|ischemia-reperfusion |
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