文章基本信息

标题：Protective Mechanism of Andrographolide against Carbon Tetrachloride-Induced Acute Liver Injury in Mice
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作者：Ju-Feng Ye ; Hang Zhu ; Zhi-Feng Zhou 等
期刊名称：Biological and Pharmaceutical Bulletin
印刷版ISSN：0918-6158
电子版ISSN：1347-5215
出版年度：2011
卷号：34
期号：11
页码：1666-1670
DOI：10.1248/bpb.34.1666
出版社：The Pharmaceutical Society of Japan
摘要：The aim of this study was to investigate the protective effects of andrographolide (AP), a bioactive component isolated from Andrographis paniculata , on carbon tetrachloride (CCl₄)-induced liver injury as well as the possible mechanisms involved in this protection in mice. Acute liver injury was induced by CCl₄ intoxication in mice. Serum biological analysis, lipid peroxides and antioxidant estimation, histopathological studies, reverse transcription polymerase chain reaction (RT-PCR) and Western blot assay were carried out. CCl₄ treatment resulted in severe hepatic injury, as evidenced by significant elevation of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels and typical histopathological changes, such as hepatocyte necrosis. Additionally, CCl₄ administration led to oxidative stress in mice, as indicated by a remarkable increase in the hepatic malondialdehyde (MDA) level, together with a significant decrease in liver reduced glutathione (GSH) content. However, CCl₄-induced hepatotoxicity was significantly attenuated by pretreatment with AP, as demonstrated by significant reduction of serum ALT, AST levels and hepatic MDA activity, along with a remarkable increase in hepatic GSH content. Histopathological changes induced by CCl₄ were also ameliorated by AP pretreatment. The marked increase of tumor necrosis factor-α (TNF-α) induced by CCl₄ was attenuated by AP, and the dramatic elevation of heme oxygenase-1 (HO-1) at transcriptional and protein levels was augmented following AP pretreatment. AP can effectively prevent liver injury induced by CCl₄, which may be due to inhibition of oxidative stress and inflammatory responses.
关键词：carbon tetrachloride;andrographolide;liver injury;inflammation;heme oxygenase-1