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天然化合物通过影响肝星状细胞自噬抗肝纤维化的研究进展。

Research progress of natural compounds in anti-liver fibrosis by affecting autophagy of hepatic stellate cells.

机构信息

Department of Gastroenterology, GuangZhou Red Cross Hospital, Jinan University, Guangzhou, 510220, China.

出版信息

Mol Biol Rep. 2021 Feb;48(2):1915-1924. doi: 10.1007/s11033-021-06171-w. Epub 2021 Feb 20.

Abstract

Chronic liver diseases caused by various pathogenesis are marked by inflammatory infiltration and wound healing reaction, while their normal regeneration ability is impaired. The unbalance between the generation and the degradation of extracellular matrix (ECM) leads to collagen accumulation and develops into liver fibrosis. Inflammation, oxidative stress, and autophagy interact closely in the pathogenesis of hepatic fibrosis. Reactive Oxygen Species (ROS) can not only stimulate Kupffer cells to release massive inflammatory factors, but induce autophagy. However, the latter may suppress inflammatory reaction by inhibiting proinflammatory complex formation directly, and removing damaged organelles or pathogenic microorganism indirectly. At present, effective anti-fibrosis drugs are still lacking. Previous studies have found various natural compounds enabled liver protection through anti-inflammatory, antioxidant, and other mechanisms. In recent years, autophagy, a vital life activity, has been found to be involved in the mechanism of liver fibrosis. As a new target, developing anti-liver fibrosis drugs that regulate the activity of autophagy is very promising. In this review, we summarize the latest studies about natural compounds in the treatment of liver fibrosis by regulating autophagy.

摘要

由各种病因引起的慢性肝脏疾病的特征是炎症浸润和伤口愈合反应,而其正常的再生能力受到损害。细胞外基质(ECM)的产生和降解之间的失衡导致胶原积累并发展为肝纤维化。在肝纤维化的发病机制中,炎症、氧化应激和自噬密切相互作用。活性氧(ROS)不仅可以刺激枯否细胞释放大量炎症因子,还可以诱导自噬。然而,后者可以通过直接抑制促炎复合物的形成,间接地清除受损的细胞器或病原体,从而抑制炎症反应。目前,有效的抗纤维化药物仍然缺乏。先前的研究发现,各种天然化合物通过抗炎、抗氧化等机制实现肝脏保护。近年来,自噬作为一种重要的生命活动,被发现参与了肝纤维化的机制。作为一个新的靶点,开发通过调节自噬活性来治疗肝纤维化的抗肝纤维化药物具有广阔的前景。在本文中,我们总结了最近关于天然化合物通过调节自噬治疗肝纤维化的研究。

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