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作 者:何胜夫(综述) 汪余勤(审校)[1] He Shengfu;Wang Yuqin(Department of Gastroenterology,XinHua Hospital,JiaoTong University School of Medicine,Shanghai 200092 China)
机构地区:[1]上海交通大学医学院附属新华医院消化内科,上海市200092
出 处:《实用肝脏病杂志》2020年第6期919-922,共4页Journal of Practical Hepatology
基 金:江苏省科技厅科研基金资助项目(编号:2017134)。
摘 要:胆汁酸由肝脏产生,是胆汁的主要成分之一。在胆汁分泌受阻时,血清和肝脏胆汁酸浓度上升,进而导致肝损害。尽管过去对于胆汁酸导致肝损害有过很多研究,但是其导致肝损害的分子机制目前仍存在争议。在本文中,我们总结了胆汁酸导致肝损伤发病机制的最新研究进展。在病理条件下,胆汁酸诱导肝细胞损害是通过处于应激条件下的肝细胞诱导炎症反应而发生的。本文主要聚焦胆汁酸如何诱导炎症因子的产生从而进一步诱导相关免疫细胞的聚集,以及基于对这些病理基础的认识,他们探讨了可能对胆汁淤积性肝损害有潜在治疗的新方法。Objective Bile acid(BA)is synthesized in the liver and is the major component of bile.BAs accumulates in serum and liver when BAs secretion is impaired,which is followed by liver injury.The molecular mechanism of cholestasis has been extensively studied,however,it remains controversial.Recent studies showed that BAs might induce hepatocyte injury under pathological conditions,and the mechanism involved inflammatory response induced by stressed hepatocytes.In this article,we reviewed recent advances in the pathogenesis of liver injury induced by BAs and we focused on how BAs induce the activation of inflammatory cytokines that further induce the aggregation of immune cells.Based on these pathogenesis,we tentatively point out a number of novel treatments for cholestatic liver damage.
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