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茵陈蒿汤对胆汁淤积性肝纤维化大鼠内质网应激PERK通路的影响 被引量:12
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作者 李木松 张贵贤 +1 位作者 魏媛媛 刘震霞 《中国中医药科技》 CAS 2016年第5期535-538,共4页
目的:观察茵陈蒿汤对胆汁淤积性肝纤维化大鼠PKR样内质网激酶(PERK)-真核生物翻译起始因子(e IF2α)-转录活性因子4(ATF4)的影响,探讨茵陈蒿汤抗胆汁淤积性肝纤维的作用机制。方法:将35只SD大鼠分为假手术组和造模组,采用胆总管结扎法... 目的:观察茵陈蒿汤对胆汁淤积性肝纤维化大鼠PKR样内质网激酶(PERK)-真核生物翻译起始因子(e IF2α)-转录活性因子4(ATF4)的影响,探讨茵陈蒿汤抗胆汁淤积性肝纤维的作用机制。方法:将35只SD大鼠分为假手术组和造模组,采用胆总管结扎法复制胆汁淤积性肝纤维化大鼠模型,1 W后将造模组动物分为模型组和中药组,中药组予以3.5 g/kg茵陈蒿汤灌胃,4 W后处死动物。HE、Masson染色观察肝脏组织病理学变化;Western blot法检测各组大鼠肝脏PERK、e IF2α和ATF4蛋白表达的变化。结果:肝脏组织病理学变化显示模型组大鼠肝纤维化程度较假手术组明显增加(P<0.05),中药组大鼠肝纤维化程度较模型组减轻(P<0.05),但仍重于假手术组。Western blot结果显示,模型组肝脏PERK、e IF2α和ATF4蛋白的表达与假手术组相比显著升高(P<0.01),中药组较模型组PERK、e IF2α和ATF4蛋白表达明显降低(P<0.01)。结论:抑制PERK、e IF2α和ATF4的活化,从而减少肝细胞凋亡,进而抑制内质网应激在胆汁淤积性肝纤维化中的促进作用,是茵陈蒿汤抗胆汁淤积性肝纤维化的作用机制之一。 展开更多
关键词 肝硬化 胆汁性 菌陈蒿汤 @内质网激酶 大鼠
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Altered expression of micro RNAs in the response to ER stress
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作者 戴丽敏 黄川 +2 位作者 陈亮 单革 李兆勇 《Science Bulletin》 SCIE EI CAS CSCD 2015年第2期202-209,I0002,共9页
MicroRNAs, a class of small noncoding RNAs, play key roles in diverse biological and pathological processes. ER stress, resulting from the accumulation of unfolded or misfolded proteins in the ER lumen, is triggered b... MicroRNAs, a class of small noncoding RNAs, play key roles in diverse biological and pathological processes. ER stress, resulting from the accumulation of unfolded or misfolded proteins in the ER lumen, is triggered by various physiological events and pathological insults. Here, using RNA deep sequencing analysis, we found that the expression of some microRNAs was altered in HeLa and HEK293 cells under ER stress. Protein and RNA levels of DGCR8, Drosha, Exportin-5, Dicer, and Ago2 showed no significant alteration in ER-stressed cells, which suggested that the change in microRNA expression might not be caused by the microRNA biogenesis pathway but by other, unknown factors. Real-time PCR assays confirmed that hsa-miR-423-5p was up-regulated, whereas hsa-miR-221-3p and hsa-miR-452-5p were down-regulated, in both HeLa and HEK293 cells under ER stress. Luciferase activity and Western blot assays verified that CDKN1A was a direct target of hsa-miR-423-5p and that CDKN1B was a direct target of hsa-miR-221-3p and hsamiR-452-5p. We speculated that by regulating their targets, microRNAs might function cooperatively as regulators in the adaptive response to ER stress. 展开更多
关键词 MICRORNA Noncoding RNA ER stress UPR
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