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作 者:叶蕾[1] 陈芝芸[1] 严茂祥[1] 赵振中[1] 李剑霜[1]
机构地区:[1]浙江中医药大学第一临床医学院,浙江省中医院,浙江杭州310006
出 处:《中华中医药学刊》2013年第12期2748-2750,共3页Chinese Archives of Traditional Chinese Medicine
基 金:浙江省中医药重点研究计划资助项目(2006Z0060);浙江省教育厅科研资助项目(Y201223352)
摘 要:目的:观察CCl4诱导的肝纤维化大鼠肝组织MAPKs信号通路的ERK通路、JNK通路、P38MAPK信号通路的变化,探讨其作用和意义。方法:采用40%CCl4皮下注射建立大鼠肝纤维化模型,采用实时荧光定量PCR技术检测肝组织MAPKs信号通路的关键信号分子ERK1、JNK2、P38基因的mRNA表达;采用Western blot技术检测大鼠肝组织ERK1/2、JNK2、P38的总蛋白表达及磷酸化水平。结果:模型大鼠肝组织ERK1、JNK2、P38基因的mRNA表达较正常组明显增强,磷酸化的ERK1/2、JNK2、P38蛋白水平也较正常组显著增加。结论:肝纤维化大鼠肝组织MAPK信号途径中的ERK、JNK及p38MAPK三条信号通路均被激活,参与了肝纤维化的进展。Objective :To observe the change of ERK signaling pathway, JNK signaling pathway and P38MAPK signa- ling pathway of liver MAPKs signaling pathway in rats with liver fibrosis induced by CC14 , and to explore the effect and significance. Methods : The model with liver fibrosis was induced by intraperitoneal injection 40% CCI4. The gene mRNA of ERK1 ,JNK2 and P38 ,which were key signaling molecules of MAPKs signaling pathway,were detected with RT - PCR; the total protein expressions and the phosphorylation levels of ERK1 ,JNK2 and P38 were detected with Western blot. Re- sults: The mRNA expression of hepatic ERK1 ,JNK2 and P38 in models were obviously enhanced than those in the normal group. And the phosphorylation protein expressions of ERK1/2 ,JNK2 and P38 were also significantly enhanced than that in the normal group. Conclusion: ERK,JNK and p38MAPK signaling pathways of liver MAPKs signaling pathway in rats with liver fibrosis were all activated, involving in the progression of liver fibrosis.
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