Obeticholic acid protects against carbon tetrachloride-induced acute liver injury and inflammation

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• 作者：Da-Gang Zhang^a ; ¹ ; Cheng Zhang^b ; ¹ ; Jun-Xian Wang^a ; Bi-Wei Wang^b ; Hua Wang^b ; Zhi-Hui Zhang^b ; Yuan-Hua Chen^b ; Yan Lu^c ; Li Tao^c ; Jian-Qing Wang^c ; Xi Chen^a ; ; De-Xiang Xu^b ; ^{xudex@126.com}
• 关键词：CCl4 ; carbon tetrachloride ; CDCA ; chenodeoxycholic acid ; ERK ; extracellular regulated protein kinase ; FXR ; farnesoid X receptor ; IkB ; inhibitor of kB ; IL ; interleukin ; KC ; keratinocyte-derived chemokine ; MAPK ; mitogen-activated protein kinase ; MCP-1 ; monocyte chemotactic protein 1 ; MIP ; macrophage inflammatory protein ; NF-κB ; nuclear factor kappa B ; OCA ; obeticholic acid ; TNF-α ; tumor necrosis factor alpha ; TUNEL ; terminal dUTP nick-end labeling ; UDCA ; ursodeoxycholic acid
• 刊名：Toxicology and Applied Pharmacology
• 出版年：2017
• 出版时间：1 January 2017
• 年：2017
• 卷：314
• 期：Complete
• 页码：39-47
• 全文大小：1297 K
• 卷排序：314

文摘

OCA pretreatment activates hepatic FXR. FXR activation protects against CCl4-induced acute liver injury. FXR activation inhibits hepatocyte apoptosis during CCl4-induced liver injury. FXR activation differentially regulates hepatic inflammatory genes. Synthetic FXR agonists are effective antidotes for acute liver injury.