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机构地区:[1]江苏大学医学院,江苏镇江212013 [2]江苏大学附属镇江三院肝病科,江苏镇江212005
出 处:《江苏大学学报(医学版)》2017年第4期301-304,共4页Journal of Jiangsu University:Medicine Edition
摘 要:目的:观察上调miR-26a-5p表达对TGF-β1刺激的LX-2肝星状细胞纤维化的影响。方法:将miR-26a-5p模拟物转染至LX-2细胞,经过TGF-β1诱导24 h,采用荧光定量PCR检测LX-2细胞内miR-26a-5p和纤维化标志物α平滑肌肌动蛋白(α-SMA)、胶原蛋白Ⅰ的mRNA表达水平;采用蛋白质印迹法检测细胞内纤维化相关蛋白pP38MAPK,α-SMA,胶原蛋白Ⅰ的表达。结果:上调miR-26a-5p表达后,LX-2细胞中α-SMA和胶原蛋白ⅠmRNA表达均明显下降(均P<0.05);p-P38MAPK,α-SMA,胶原蛋白的表达亦明显下降(均P<0.05)。结论:miR-26a-5p表达上调可抑制肝星状细胞TGF-β/P38MAPK通路,产生抗纤维化作用。Objective: To observe the effects of miR-26a-5p on fibrosis in human hepatic stellate cell LX-2. Methods: The miR-26a-5p mimics were transfected into LX-2 cells. Then the transfected cells were induced by TGF-β1for 24 hours. The expressions of miR-26a-5p,α-SMA mRNA and Collagen ⅠmRNA were detected with real-time PCR. And the expressions of fibrosis related protein p-P38 MAPK,α-SMA and CollagenⅠwere detected with the Western blotting. Results: By up-regulating the expression of miR-26a-5p,the expressions of α-SMA mRNA,CollagenⅠmRNA and the expressions of fibrosis related protein( p-P38 MAPK,α-SMA and Collagen Ⅰ) decreased compared to the control group. Conclusion:Upregulation of miR-26a-5p may inhibit the TGF-β/P38 MAPK signaling pathway in the LX-2 cells. And miR-26a-5p may play a role in anti-fibrosis.
关 键 词:miR-26a-5p 肝纤维化 TGF-β/P38MAPK通路 肝星状细胞
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