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KMID : 1034820210170020161
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Molecular & Cellular Toxicology
2021 Volume.17 No. 2 p.161 ~ p.168
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Prevention of acetaminophen-induced hepatocyte injury: JNK inhibition and GSTA1 involvement
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Chang Yicong
He Jingshan
Ishfaq Muhammad
Wang Jiaqi
Zhang Ruichen
Yuan Liang
Liu Jiarui
Li Changwen
Liu Fangping
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Abstract
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Background: Glutathione S-transferase A1 (GSTA1) is a detoxification enzyme and a sensitive marker for hepatotoxicity. We investigated the effects of JNK inhibition on different degrees of Acetaminophen (APAP)-induced hepatocyte injury and GSTA1 expression.
Objective: This study aimed to investigate the role of JNK signaling pathway in APAP-induced different degrees of hepatocyte injury and its correlation with GSTA1 by inhibiting the phosphorylation of JNK by SP600125.
Results: 6 and 8 mM APAP induced different degrees of hepatocyte injury and apoptosis, both activated JNK signaling pathway. In contrast, JNK inhibitor significantly reduced activation of JNK and c-JUN on exposure to APAP. Meanwhile, the levels of hepatocyte injury, oxidative stress, and apoptosis obviously decreased. Importantly, GSTA1 expression was significantly increased by JNK inhibition.
Conclusions: JNK inhibition attenuates APAP-induced hepatocyte injury and oxidative stress and increases GSTA1 expression. Furthermore, GSTA1 may be involved in this signaling pathway for detoxification.
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KEYWORD
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JNK, GSTA1, Acetaminophen, SP600125, Hepatocyte injury
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