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鞣花酸通过抑制线粒体活性氧的产生来保护肝细胞免受损伤。

Ellagic acid protects hepatocytes from damage by inhibiting mitochondrial production of reactive oxygen species.

机构信息

Liver cell Signal Transduction Lab., Metabolic Syndrome Research Division, Korea Research Institute of Bioscience and Biotechnology, PO Box 115, 52, Eoundong, Yusong 305-606, Republic of Korea.

出版信息

Biomed Pharmacother. 2010 Apr;64(4):264-70. doi: 10.1016/j.biopha.2009.06.013. Epub 2009 Oct 23.

Abstract

The aim of this experiment is to investigate the antioxidative and antiapoptotic roles of ellagic (EA) acid in in vitro and in in vivo experiment. We measured protective properties of EA against oxidative stress-induced hepatocyte damage in vitro and Concanavalin (ConA)-induced liver damage in vivo. EA, a potent antioxidant, exhibited protective properties against oxidative stress-induced hepatocyte damage by preventing vitamin k3 (VK3)-induced reactive oxygen species (ROS) productions, apoptotic and necrotic cellular damage and mitochondrial depolarization, which is a main cause of ROS production. EA also protects against cell death and elevation of glutathione (GSH), alanine transaminase (ALT) and asparatate transaminase (AST) in Con A-induced fulminant liver damage in mice. These results show that antioxidant and cytoprotective properties of EA prevent liver damage induced by various type of oxidative stress.

摘要

本实验旨在研究鞣花酸(EA)在体外和体内实验中的抗氧化和抗凋亡作用。我们测量了 EA 对体外氧化应激诱导的肝细胞损伤和体内 Concanavalin(ConA)诱导的肝损伤的保护作用。EA 作为一种有效的抗氧化剂,通过防止维生素 K3(VK3)诱导的活性氧(ROS)产生、凋亡和坏死细胞损伤以及线粒体去极化,表现出对氧化应激诱导的肝细胞损伤的保护作用,线粒体去极化是 ROS 产生的主要原因。EA 还可防止细胞死亡和谷胱甘肽(GSH)、丙氨酸转氨酶(ALT)和天冬氨酸转氨酶(AST)在 ConA 诱导的小鼠暴发性肝损伤中的升高。这些结果表明,EA 的抗氧化和细胞保护特性可预防各种类型的氧化应激引起的肝损伤。

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