乙醛
肿瘤坏死因子α
对乙酰氨基酚
氧化应激
药理学
乙醇代谢
CYP2E1
化学
阿尔法(金融)
发病机制
乙醇
生物
细胞色素P450
免疫学
医学
生物化学
新陈代谢
护理部
患者满意度
结构效度
作者
Wenyan Xie,Jianguo Sun,Xiaoying Zhang,MF Melzig
出处
期刊:PubMed
日期:2014-05-01
卷期号:69 (5): 379-84
被引量:7
摘要
The liver plays an essential role in xenobiotic metabolism including alcohol and drugs. Oxidative stress that usually occurs during the hepatic metabolism participates in the pathogenesis of liver disease. Inflammatory cytokines that exist in liver in both physiological and pathophysiological conditions may change the hepatic toxic response to hepatotoxicants. The human hepatoma cell line HepG2 is frequently used as in vitro model for biomedical studies. In this work, HepG2 cells were pre-incubated with or without TNF-alpha, and then treated with ethanol, acetaldehyde, acetaminophen and tert-butyl hydroperoxide, respectively. Cell viability was measured by MTT assay. The data showed that HepG2 cells were generally resistant to xenobiotic compounds, especially to alcohol and acetaldehyde, which may be partially caused by the absence of specific cytochrome P450 systems in these cells. TNF-alpha could sensitize the toxic response of HepG2 cells to those exogenous compounds, indicating the important role of TNF-alpha in the pathogenesis of alcohol, drugs and oxidant related liver diseases.
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