TLR4 / NF-κB 通路对非酒精性脂肪肝的作用机制

目的探讨TLR4／NF—KB信号通路调控铁调素在非酒精性脂肪肝发病中的作用机制。方法60只SD大鼠，随机分为正常组、模型组和干预组。模型组予高脂饮食制备NAFLD大鼠模型，以TLR4／NF—KB信号通路抑制剂腹腔注射干预组大鼠。处死各组大鼠，观察各组肝组织病理变化，检测TLR4、NF—KB蛋白的表达及铁调素mR—NA水平的表达。结果模型组大鼠肝脏呈现典型脂肪性变，其TLR4、NF—KB蛋白表达及铁调素mRNA水平显著高于正常组（P〈0．05）。干预组大鼠肝组织病理改变显著改善，TLR4、NF—KB蛋白表达及铁调素mRNA水平显著下降（P〈0．05）。结论TLR4／NF—KB信号通路的异常激活可能上调铁调素表达，参与了非酒精性脂肪肝的发生。

Mechanism of iron metabolism in nonalcoholic fatty liver disease adjusted by TLR4/Nf-kB signal pathway

Objective To investigate the mechanism of Hepcidin in non-alcoholic fatty liver disease （NAFLD） adjusted by TLR4/NF-kB signal pathway. Methods Sixty SD rats were divided into normal, model and intervention group. A NAFLD rat model was created using high-fat diet fed. Pathenolide was injected intraperitoneally in the intervention group. Pathological changes of hepatic tissues were observed under microscope. The expression of TLR4 and NF-KB protein in hepatic tissues and the expression of hepcidin mRNA was determined by RT-PCR. Results The typical fatty degeneration occurred in the livers of rats in the model group. The levels of TLR4 and NF-KB protein and hepcidin mRNA were significantly higher than those in the normal group（P 〈 0.05）. The pathologic change of liver tissues of rats in the intervention group was improved obviously,the levels of TLR4 and NF-KB protein and hepcidin mRNA decreased significantly（ P 〈 0. 05 ）. Conclusion The abnormal activation of TLR4/NF-KB signal pathway may be responsible for the up regulation of Hepcidin expression and the occurrence of NAFLD.