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Thunb.提取物对乙酰氨基酚诱导的肝毒性的保护作用及可能的分子机制。

Protective effects and possible molecular mechanism of Thunb. extract on acetaminophen-induced hepatotoxicity.

作者信息

Dong Sijing, Ji Jianbo, Zhang Baofang, Hu Lingyun, Cui Xiangzhen, Wang Haina

出版信息

Pharmazie. 2018 Nov 1;73(11):666-670. doi: 10.1691/ph.2018.8650.

DOI:10.1691/ph.2018.8650
PMID:30396387
Abstract

Thunb. is a traditional hepatoprotective Chinese medicine, and in research, much effort has been focused on the protection against alcoholic liver injury. In this study, the protective effects of a fruit ethanol extract of (FE) against APAP-induced acute hepatotoxicity in mice and the possibly involved molecular mechanisms were investigated. Hepatoprotective activity of FE is clearly indicated by histopathological and biochemical examination. Treatment with FE resulted in inhibition of CYP2E1 activity involved in the transformation of APAP . Expressions of the altered bile acid metabolism and transport-related genes and relative proteins of apoptosis were normalized by preconditioning with FE before APAP treatment. These results suggested FE to alleviate APAP-induced liver injury in a dose-dependent manner by inhibition of cytochrome P450 activity, hepatocyte apoptosis and regulation of bile acid homeostasis imbalance.

摘要

茵陈是一种传统的保肝中药,在研究中,很多努力都集中在对酒精性肝损伤的保护上。在本研究中,研究了茵陈果实乙醇提取物(FE)对乙酰氨基酚诱导的小鼠急性肝毒性的保护作用以及可能涉及的分子机制。组织病理学和生化检查清楚地表明了FE的保肝活性。FE处理导致参与乙酰氨基酚转化的CYP2E1活性受到抑制。在乙酰氨基酚处理前用FE预处理可使胆汁酸代谢和转运相关基因以及凋亡相关蛋白的表达恢复正常。这些结果表明,FE通过抑制细胞色素P450活性、肝细胞凋亡和调节胆汁酸稳态失衡,以剂量依赖的方式减轻乙酰氨基酚诱导的肝损伤。

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