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The Model of Acute Liver Injury Induced by Acetaminophen in Mice
Li Dawei1, Lu Tianfei1, Hua Xiangwei1, Zhang Jianjian1, Wang Weigang2, Cui Xiaolan1, Dai Huijuan1, Zhang Ming1, Xia Qiang1*
1Department of Liver Surgery, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200127, China; 2Shanghai Research Center of Model Organisms, Shanghai 201203, China
Abstract: The aim of the study was to improve the acute liver injury model and lethal model of mice induced
by acetaminophen (APAP) injection. 20 mice were divided into 4 groups randomly: normal control， APAP 3 h group， APAP 6 h group， and APAP 12 h group. Mice were fasted for 15 hours before APAP injection to induce liver injury. We assayed serum alanine aminotransferase (ALT)， aspartate aminotransferase (AST) and examined liver pathologic changes after APAP injection by HE staining. 20 mice were divided into four groups: control group， fast+APAP (500 mg/kg) group， fast+APAP (300 mg/kg) group and non-fast+APAP (500 mg/kg) group.The four groups were administrated at the same time. We observed the survival status of mice before and after APAP administration and made survival curve. Serum ALT and AST levels increased by time after APAP administration and were significantly higher than that in control group (P<0.05). Liver specimens of APAP mice displayed characteristic centrilobular necrosis and inflammatory infiltration. All mice of fast+APAP (500 mg/kg) group died within 16 to 72 hours， and the mortality was significantly higher than those of the other 3 groups. Our study successfully improved acute liver injury model and lethal model of C57/BL6 mice induced by APAP， which laid the foundation for further exploration of mechanism and control measures of APAP-induced hepatotoxicity.
by acetaminophen (APAP) injection. 20 mice were divided into 4 groups randomly: normal control， APAP 3 h group， APAP 6 h group， and APAP 12 h group. Mice were fasted for 15 hours before APAP injection to induce liver injury. We assayed serum alanine aminotransferase (ALT)， aspartate aminotransferase (AST) and examined liver pathologic changes after APAP injection by HE staining. 20 mice were divided into four groups: control group， fast+APAP (500 mg/kg) group， fast+APAP (300 mg/kg) group and non-fast+APAP (500 mg/kg) group.The four groups were administrated at the same time. We observed the survival status of mice before and after APAP administration and made survival curve. Serum ALT and AST levels increased by time after APAP administration and were significantly higher than that in control group (P<0.05). Liver specimens of APAP mice displayed characteristic centrilobular necrosis and inflammatory infiltration. All mice of fast+APAP (500 mg/kg) group died within 16 to 72 hours， and the mortality was significantly higher than those of the other 3 groups. Our study successfully improved acute liver injury model and lethal model of C57/BL6 mice induced by APAP， which laid the foundation for further exploration of mechanism and control measures of APAP-induced hepatotoxicity.
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