鞘脂
MAPK/ERK通路
肝损伤
药理学
信号转导
生物
氧化应激
代谢途径
代谢组学
转录组
激酶
炎症
生物化学
化学
新陈代谢
免疫学
生物信息学
基因表达
基因
作者
Wuchang Zhu,Hongmei Su,Yuansong Wei,Yushen Huang,Siyun Chen,Yanxia Shi,Ling Yan,Yue Qiu,Jinbin Wei
摘要
Abstract In this study, we aimed to determine whether asiatic acid (AA) exerts any therapeutic effects on rifampicin (RFP)‐ and isoniazid (INH)‐induced liver injury and elucidate the underlying mechanisms. Briefly, liver injury in mice was induced via RFP and INH administration. We investigated the effects and potential action mechanisms of AA on liver injury using transcriptomics, metabolomics and various examinations. We found that AA significantly ameliorated the pathological changes in liver tissues and decreased the transaminase activity, inflammation and oxidative stress damage. Transcriptomics revealed 147 differentially expressed genes (DEGs) between the AA and model groups that were enriched in metabolic and mitogen‐activated protein kinase ( MAPK ) signalling pathways. Metabolomics revealed 778 differentially expressed metabolites between the AA and model groups. Furthermore, integrated transcriptomics and metabolomics analyses revealed strong correlations between DEGs and differentially expressed metabolites and indicated that AA regulates the sphingolipid metabolism by inhibiting the expression of delta 4‐desaturase, sphingolipid 1. Experimental results confirmed that AA inhibited the MAPK signalling pathway. In summary, AA inhibits inflammation and oxidative stress damage by regulating the sphingolipid metabolism pathway and blocking the MAPK signalling pathway, thereby relieving the RFP/INH‐induced liver injury.
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