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.

中文翻译：

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预防对乙酰氨基酚引起的肝细胞损伤：JNK抑制和GSTA1参与

背景

谷胱甘肽S-转移酶A1（GSTA1）是一种解毒酶，是肝毒性的敏感标志物。我们研究了JNK抑制对不同程度对乙酰氨基酚（APAP）诱导的肝细胞损伤和GSTA1表达的影响。

目的

本研究旨在通过抑制SP600125抑制JNK的磷酸化来研究JNK信号通路在APAP诱导的不同程度肝细胞损伤中的作用及其与GSTA1的相关性。

结果

6和8 mM APAP诱导了不同程度的肝细胞损伤和凋亡，均激活了JNK信号通路。相反，JNK抑制剂在暴露于APAP时显着降低JNK和c-JUN的活化。同时，肝细胞损伤，氧化应激和凋亡水平明显降低。重要的是，JNK抑制可显着增加GSTA1表达。

结论

JNK抑制可减弱APAP诱导的肝细胞损伤和氧化应激并增加GSTA1表达。此外，GSTA1可能参与此信号通路进行解毒。