Indole-3-carboxaldehyde alleviates acetaminophen-induced liver injury via inhibition of oxidative stress and apoptosis

作者全名：Liu, Xinlei; Liu, Rui; Wang, Yancheng

作者地址：[Liu, Xinlei] Chongqing Univ, Lab Anim Res Ctr, Sch Med, Chongqing 400044, Peoples R China; [Liu, Xinlei] Chongqing Univ, Stem Cell Res Ctr, Sch Med, Chongqing 400044, Peoples R China; [Liu, Rui] Chongqing Med Univ, Inst Immunol Innovat & Translat, Chongqing, Peoples R China; [Wang, Yancheng] Chongqing Univ, Sch Elect Engn, State Key Lab Power Transmiss Equipment Technol, 174 Shazhengjie Rd, Chongqing 400044, Peoples R China

通信作者：Wang, YC (通讯作者)，Chongqing Univ, Sch Elect Engn, State Key Lab Power Transmiss Equipment Technol, 174 Shazhengjie Rd, Chongqing 400044, Peoples R China.

来源：BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS

ESI学科分类：BIOLOGY & BIOCHEMISTRY

WOS号：WOS:001223173800001

JCR分区：Q3

影响因子：2.5

年份：2024

卷号：710

期号：　

开始页：　

结束页：　

文献类型：Article

关键词：Acetaminophen; Liver injury; Indole-3-carboxaldehyde; Oxidative stress; Apoptosis

摘要：Drug-induced liver injury (DILI) occurs frequently and can be life-threatening. Increasing researches suggest that acetaminophen (APAP) overdose is a leading cause of drug-induced liver injury. Indole-3-carboxaldehyde (I3A) alleviates hepatic inflammation, fibrosis and atherosclerosis, suggesting a potential role in different disease development. However, the question of whether and how I3A protects against acetaminophen-induced liver injury remains unanswered. In this study, we demonstrated that I3A treatment effectively mitigates acetaminophen-induced liver injury. Serum alanine/aspartate aminotransferases (ALT/AST), liver malondialdehyde (MDA) activity, liver glutathione (GSH), and superoxide dismutase (SOD) levels confirmed the protective effect of I3A against APAP-induced liver injury. Liver histological examination provided further evidence of I3Ainduced protection. Mechanistically, I3A reduced the expression of apoptosis-related factors and oxidative stress, alleviating disease symptoms. Finally, I3A treatment improved survival in mice receiving a lethal dose of APAP. In conclusion, our study demonstrates that I3A modulates hepatotoxicity and can be used as a potential therapeutic agent for DILI.

基金机构：National Natural Science Foundation of China [51877022, 51807016]; Fundamental Research Funds for the Central Universities

基金资助正文：This work was supported in part by the National Natural Science Foundation of China under Grant 51877022 and 51807016, in part by the Fundamental Research Funds for the Central Universities