Expression of glutathione S-transferase A1, a phase II drug-metabolizing enzyme in acute hepatic injury on mice
文献类型: 外文期刊
第一作者: Ma, Xin
作者: Ma, Xin;Liu, Fangping;Li, Minmin;Li, Zhi;Lin, Yuexia;Li, Rui;Chang, Yicong;Zhao, Changwei;Han, Qing;Zhou, Qiong;Zhao, Yulin;Wang, Dening;Li, Changwen;Liu, Jingli
作者机构:
关键词: glutathione S-transferase A1;acute hepatic injury;content;mRNA expression;antioxidant
期刊名称:EXPERIMENTAL AND THERAPEUTIC MEDICINE ( 影响因子:2.447; 五年影响因子:2.263 )
ISSN: 1792-0981
年卷期: 2017 年 14 卷 4 期
页码:
收录情况: SCI
摘要: In the present study, three models of acute liver injury in mice were induced via the administration of CCl4 (35 mg/kg, 24 h), acetyl-para-aminophenol (APAP; 200 mg/kg, 12 h) and ethanol (14 ml/kg, 8 h) to study the effect of glutathione S-transferase A1 (GSTA1) on acute liver injury. The serum levels of alanine transaminase, aspartate transaminase and liver homogenate indicators (superoxide dismutase, glutathione and glutathione peroxidase) were significantly lower in model groups compared with the control group (P<0.01), whereas the liver homogenate indicator malondialdehyde was significantly increased (P<0.01). The expression of GSTA1 in liver was significantly decreased in the model groups compared with the control group (P<0.01). GSTA1 protein content was 3.8, 1.3 and 2.6 times lower in the CCl4, APAP and ethanol model groups, respectively. Furthermore, GSTA1 mRNA expression levels decreased by 4.9, 2.1 and 3.7 times in the CCl4, APAP and ethanol model groups, respectively. Among the three models, the injury induced by CCl4 was the most marked, followed by ethanol and finally APAP. These results suggest that GSTA1 may be released by the liver and serve as an antioxidant in the prevention of liver damage.
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