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目的:探讨加味泽泻汤对高脂饮食诱导的大鼠非酒精性脂肪肝(NAFLD)模型的治疗机制。方法:SPF级大鼠分为空白组、模型组、加味泽泻汤组、多烯磷脂酰胆碱组,大鼠分别以10%或45%高脂纯化饲料喂养12周构建NAFLD模型。加味泽泻汤及多烯磷脂酰胆碱治疗组分别给药4周,空白组及模型组则给予相应体积双蒸水4周。以蛋白免疫印迹(Western blot)法检测Toll样受体4(TLR4),髓样分化因子88(My D88),核转录因子-κB p65(NF-κB p65),p38丝裂原活化蛋白酶(p38MAPK),磷酸化的p38丝裂原活化蛋白酶(p-p38),c-Jun氨基末端激酶(JNK),半胱氨酸蛋白水解酶-1(Caspase-1)在大鼠肝脏中的表达。结果:与空白组比较,模型组TLR4,My D88,NF-κB p65,p-p65,p38 MAPK,p-p38,JNK及Caspase-1蛋白表达明显增高(P<0.05);而加味泽泻汤组相应蛋白的表达量较模型组均显著下降(P<0.01)。结论:在高脂饮食诱导的大鼠NAFLD模型中,加味泽泻汤通过抑制TLR4/NF-κB,MAPK信号通路相关蛋白的表达,从而抑制肝脏炎症的产生、缓解肝脏的损伤,达到治疗NAFLD的目的。
Objective: To investigate the therapeutic mechanism of Jiawei Alisma Decoction on rat model of non-alcoholic fatty liver (NAFLD) induced by high-fat diet. Methods: SPF rats were divided into blank group, model group, Jiawei Alisma Decoction group, polyene phosphatidylcholine group, and rats were respectively fed with 10% or 45% fat diet for 12 weeks to construct NAFLD model. Modified Wei Alchemy Decoction and polyene phosphatidylcholine treatment group were given for 4 weeks, the blank group and model group were given the corresponding volume of double distilled water for 4 weeks. Toll-like receptor 4 (TLR4), myeloid differentiation factor 88 (My D88), nuclear factor-κB p65 (NF-κB p65) and p38 mitogen activated protein kinase (p38 MAPK) were detected by Western blotting. ), Phosphorylated p38 mitogen-activated proteinase (p-p38), c-Jun N-terminal kinase (JNK) and caspase-1 in rat liver. Results: The expression of TLR4, My D88, NF-κB p65, p-p65, p38 MAPK, p-p38, JNK and Caspase-1 in the model group were significantly higher than those in the blank group Compared with the model group, the expression of the corresponding protein decreased significantly (P <0.01). Conclusion: In the model of NAFLD induced by high-fat diet, Jiaweizheizhitang can inhibit hepatic inflammation by inhibiting the expression of TLR4 / NF-κB and MAPK signaling pathway, relieve the liver injury and achieve the goal of treating NAFLD purpose.