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目的:观察法尼酯衍生物X受体(farnesoid X receptor,FXR)-促甲状腺素胚胎因子(thyrotropin embryonic factor,TEF)通路在自身免疫性肝炎模型小鼠肝损害中的作用,探讨FXR-TEF通路改善自身免疫性肝炎的部分可能机制。方法:检测FXR在伴刀豆球蛋白A(concanavalin A,Con A)诱导的肝炎(Con A-induced hepatitis,CIH)小鼠肝脏的表达;检测FXR激活对TEF表达的影响;观察C57BL/6小鼠和鹅去氧胆酸(chenodeoxycholic acid,CDCA)激活FXR的CIH小鼠肝脏病理、肝脏酶学及炎症因子变化。结果:FXR在CIH小鼠中低表达;CDCA激活FXR的C57BL/6小鼠TEF表达上调;FXR被激活的CIH小鼠的肝损害较轻,FXR激活可减轻肝脏炎症因子释放。结论:CDCA激活FXR能减轻CIH引起的肝功能损害和炎症反应。FXR激活使TEF上调。FXR可能是自身免疫性肝炎的保护因素,其保护作用可能是通过TEF来实现的。激活FXR可能成为治疗自身免疫性肝炎的一个途径。
OBJECTIVE: To observe the role of farnesoid X receptor (FXR) - thyrotropin embryonic factor (TEF) pathway in hepatic injury induced by autoimmune hepatitis in mice and to explore the role of FXR-TEF Pathway to improve autoimmune hepatitis may be part of the possible mechanisms. Methods: The expression of FXR in the liver of Con A-induced hepatitis (CIH) -induced hepatitis A (Con A) -induced hepatitis (CIH) mice was detected. The effect of FXR activation on the expression of TEF was observed. The expression of C57BL / 6 Changes of hepatic pathology, liver enzymes and inflammatory cytokines in CIH mice activated by chenodeoxycholic acid (CDCA) and FXR. Results: FXR was down-regulated in CIH mice; TEF expression was up-regulated in CD57-activated FXR-induced C57BL / 6 mice; liver damage in FXR-activated CIH mice was lighter, and FXR activation attenuated hepatic inflammatory cytokines release. Conclusion: Activation of FXR by CDCA can reduce the damage of liver function and inflammatory reaction induced by CIH. FXR activation up-regulates TEF. FXR may be a protective factor of autoimmune hepatitis, its protective effect may be achieved through TEF. Activation of FXR may be a way to treat autoimmune hepatitis.