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黄芩素通过调节线粒体相关凋亡对肝损伤发挥强大的保护作用。

A potent protective effect of baicalein on liver injury by regulating mitochondria-related apoptosis.

机构信息

Institute for Translational Medicine, Qingdao University, #38 Dengzhou Road, Qingdao, 266000, Shandong, People's Republic of China.

School of Basic Medicine, Qingdao University, Qingdao, People's Republic of China.

出版信息

Apoptosis. 2020 Jun;25(5-6):412-425. doi: 10.1007/s10495-020-01608-2.

DOI:10.1007/s10495-020-01608-2
PMID:32409930
Abstract

Liver injury is the early stage of liver disease, which is caused by multiple factors. Baicalein has shown extensive bioactivity. But whether baicalein has a protective effect on liver injury has not been reported thus far. In this study, we aim to investigate the protective effects of baicalein on liver injury induced by oxidative stress. HO and CCl were employed to establish liver injury models in vivo and in vitro, respectively. The protective effect of baicalein on oxidative stress-induced liver injury was evaluated by detecting the mitochondrial dynamics, the level of autophagy and apoptosis, the histopathology of liver, the indicators of liver function, and the level of oxidative stress in vitro and in vivo. March5 is the key regulator during liver injury induced by oxidative stress. March5 can ubiquitinate Drp1 and promote Drp1 degradation, then maintain the homeostasis of mitochondrial dynamics, keep the balance of autophagy, and reduce apoptosis. Baicalein is able to effectively reduce liver injury; it can contribute to the expression of March5 by regulating KLF4 during liver injury. These results indicate that baicalein plays a key role in salvaging liver from injury induced by oxidative stress via regulating the KLF4-March5-Drp1 signal pathway.

摘要

肝损伤是肝病的早期阶段,由多种因素引起。黄芩素具有广泛的生物活性。但到目前为止,还没有报道黄芩素对肝损伤是否具有保护作用。在这项研究中,我们旨在研究黄芩素对氧化应激诱导的肝损伤的保护作用。HO 和 CCl 分别用于在体内和体外建立肝损伤模型。通过检测线粒体动力学、自噬和凋亡水平、肝组织病理学、肝功能指标以及体内外氧化应激水平,评估黄芩素对氧化应激诱导的肝损伤的保护作用。March5 是氧化应激诱导肝损伤的关键调节因子。March5 可以泛素化 Drp1 并促进 Drp1 降解,从而维持线粒体动力学的平衡,保持自噬和减少凋亡的平衡。黄芩素能有效减轻肝损伤;它可以通过调节 KLF4 在肝损伤过程中表达 March5。这些结果表明,黄芩素通过调节 KLF4-March5-Drp1 信号通路,在挽救氧化应激诱导的肝损伤方面发挥关键作用。

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