Abstract:
:Acetaminophen (APAP) is a widely used over-the-counter analgesic and antipyretic. It can cause hepatotoxicity. Recent studies demonstrated that hydrogen sulfide (H2 S) exhibits cell protection in several cell types. This study was designed to investigate whether H 2 S ameliorated APAP-induced acute liver injury and to elucidate its mechanisms. In this study, we analyzed the detailed biological and molecular processes of APAP-induced hepatotoxicity using a bioinformatics analysis, which showed that apoptosis and the c-Jun N-terminal kinase (JNK)/mitogen-activated protein kinase pathway were confirmed to play critical roles in these processes. We further investigated the protective effects of H 2 S on APAP-induced hepatotoxicity. In vivo, we observed that the exogenous supplement of H 2 S ameliorated APAP-induced liver injury. Cystathionine-β-synthase (CBS) and cystathionine-γ-lyase (CSE) systems were the endogenous pathway of H 2 S. The expression of CBS/CSE was decreased in APAP-treated mice, while H 2 S could significantly restore it. In addition, APAP-induced JNK activation was inhibited by H 2 S in vivo. In vitro, H 2 S abolished the active effects of APAP on caspase3, Bax, and Bcl-2 expressions as well as JNK phosphorylation in hepatocytes. It was found through flow cytometry that the amount of APAP-induced apoptotic hepatocytes was decreased in the presence of H 2 S. In conclusion, our results suggested that H 2 S attenuated APAP-induced apoptosis in hepatocytes through JNK/MAPK siganaling pathway.
journal_name
J Cell Biochemjournal_title
Journal of cellular biochemistryauthors
Li X,Lin J,Lin Y,Huang Z,Pan Y,Cui P,Yu C,Cai C,Xia Jdoi
10.1002/jcb.27724subject
Has Abstractpub_date
2019-03-01 00:00:00pages
4385-4397issue
3eissn
0730-2312issn
1097-4644journal_volume
120pub_type
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