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目的:观察法尼酯衍生物X受体(FXR)激活是否减轻MRL/lpr狼疮小鼠肝损害。方法:检测FXR在MRL/lpr狼疮小鼠及正常BALB/c小鼠肝脏的表达;观察BALB/c小鼠和鹅去氧胆酸(CDCA)激活FXR的MRL/lpr小鼠再以伴刀豆球蛋白A(ConA)诱导肝脏炎症反应后的肝脏酶学、炎症因子及病理学的变化。结果:FXR在MRL/lpr狼疮小鼠肝脏中低表达;ConA能在MRL/lpr小鼠诱导出较对照BALB/c小鼠更严重的肝损害;激活FXR减轻MRL/lpr狼疮小鼠ConA诱导的肝脏炎症损伤,并减少一系列炎症因子的释放。结论:CDCA激活FXR后,能减轻狼疮小鼠肝脏损害。FXR可能是系统性红斑狼疮肝损害的一个保护性因素,激活FXR可能成为狼疮肝损害的一个治疗途径。
OBJECTIVE: To observe whether farnesyl ester derivative X receptor (FXR) activation attenuates liver damage in MRL / lpr lupus mice. Methods: The expression of FXR in the liver of MRL / lpr lupus mice and normal BALB / c mice was detected. MRL / lpr mice with FXR activated by BALB / c mice and chenodeoxycholic acid (CDCA) Changes of hepatic enzymology, inflammatory factors and pathology induced by ConA in liver inflammation. Results: FXR was low expressed in the livers of MRL / lpr lupus mice; ConA induced more severe liver damage in MRL / lpr mice than control BALB / c mice; activation of FXR attenuated ConA-induced MRL / lpr lupus mice Liver inflammation damage, and reduce the release of a series of inflammatory factors. Conclusion: Activation of FXR by CDCA can relieve liver damage in lupus mice. FXR may be a protective factor for hepatic damage in systemic lupus erythematosus. Activation of FXR may be a therapeutic pathway for lupus liver damage.