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谷胱甘肽S-转移酶A1(一种II相药物代谢酶)在小鼠急性肝损伤中的表达

Expression of glutathione S-transferase A1, a phase II drug-metabolizing enzyme in acute hepatic injury on mice.

作者信息

Ma Xin, Liu Fangping, Li Minmin, Li Zhi, Lin Yuexia, Li Rui, Li Changwen, Chang Yicong, Zhao Changwei, Han Qing, Zhou Qiong, Zhao Yulin, Wang Dening, Liu Jingli

机构信息

College of Veterinary Medicine, Northeast Agricultural University, Harbin, Heilongjiang 150030, P.R. China.

Harbin Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Harbin, Heilongjiang 150069, P.R. China.

出版信息

Exp Ther Med. 2017 Oct;14(4):3798-3804. doi: 10.3892/etm.2017.4957. Epub 2017 Aug 17.

Abstract

In the present study, three models of acute liver injury in mice were induced via the administration of CCl (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 CCl APAP and ethanol model groups, respectively. Furthermore, GSTA1 mRNA expression levels decreased by 4.9, 2.1 and 3.7 times in the CCl APAP and ethanol model groups, respectively. Among the three models, the injury induced by CCl 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.

摘要

在本研究中,通过给予小鼠三氯甲烷(35毫克/千克,24小时)、对乙酰氨基酚(APAP;200毫克/千克,12小时)和乙醇(14毫升/千克,8小时)诱导三种急性肝损伤模型,以研究谷胱甘肽S-转移酶A1(GSTA1)对急性肝损伤的影响。与对照组相比,模型组血清谷丙转氨酶、谷草转氨酶水平及肝匀浆指标(超氧化物歧化酶、谷胱甘肽和谷胱甘肽过氧化物酶)显著降低(P<0.01),而肝匀浆指标丙二醛显著升高(P<0.01)。与对照组相比,模型组肝脏中GSTA1的表达显著降低(P<0.01)。在三氯甲烷、APAP和乙醇模型组中,GSTA1蛋白含量分别降低了3.8倍、1.3倍和2.6倍。此外,在三氯甲烷、APAP和乙醇模型组中,GSTA1 mRNA表达水平分别下降了4.9倍、2.1倍和3.7倍。在这三种模型中,三氯甲烷诱导的损伤最为明显,其次是乙醇,最后是APAP。这些结果表明,GSTA1可能由肝脏释放,并作为一种抗氧化剂预防肝损伤。

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