鸡骨草提取物对非酒精性脂肪肝大鼠肝细胞TLR4/p38MAPK信号通路作用

Effect of Abrus mollis Hance on TLR4/p38MAPK signal pathway in liver cells of nonalcoholic fatty liver disease rats

目的研究鸡骨草提取物对非酒精性脂肪肝(NAFLD)大鼠肝细胞TLR4/p38MAPK信号通路的影响。方法长期饲喂高脂饲料建立NAFLD模型,设空白对照组、模型组、辛伐他汀组、鸡骨草水提物高剂量组(15 g/kg)、鸡骨草水提物中剂量组(10 g/kg)、鸡骨草水提物低剂量组(5 g/kg)、鸡骨草50%醇提物高剂量组(15 g/kg)、鸡骨草50%醇提物中剂量组(10 g/kg)、鸡骨草50%醇提物低剂量组(5 g/kg),利用生化分析仪测定血脂、炎症因子指标,并采用PCR和Western blot法测定肝组织TLR4、p38MAPK蛋白表达。结果与模型组比较,鸡骨草水提物与50%醇提物中、高剂量组大鼠肝组织三酰甘油(TG)、总胆固醇(TC)、低密度脂蛋白胆固醇(LDL-C)、游离脂肪酸(FFA)水平显著降低(P<0.01),高密度脂蛋白胆固醇(HDL-C)水平升高(P<0.05或P<0.01);鸡骨草水提取物与50%醇提物中、高剂量组大鼠血清白介素1(IL-1)、白介素6(IL-6)、肿瘤坏死因子α(TNF-α)水平降低(P<0.05或P<0.01);鸡骨草水提取物与50%醇提物中、高剂量组大鼠肝组织Toll样受体蛋白4(TLR4)、p38丝裂原活化蛋白激酶(p38MAPK)mRNA表达量降低(P<0.05或P<0.01)。结论鸡骨草通过调节TLR4/p38MAPK信号通路,发挥抗炎和改善脂质代谢紊乱作用。

Objective To study the effect of Abrus mollis Hance on TLR4/p38MAPK signal pathway in liver cells of nonalcoholic fatty liver disease （ NAFLD） rats. Methods The rat model of NAFLD was established by long-term feeding of high-fat diets. The rats were divided into 9 groups, including the blank control group,the model group, simvastatin group, three different doses （ 5, 10 and 15 g/kg ） of aqueous Abrus mollis Hance extract groups,and three different doses （ 5,10 and 15 g/kg） of 50% alcohol Abrus mollis Hance extract groups. The levels of serum lipids and inflammatory factors were determined by biochemical analyzer. The expression of TLR4 and p38MAPK in liver tissue was assayed by PCR and Western blot. Results Compared with the model group,aqueous extract groups and 50% alcohol high- and middle-dose extract groups significantly reduced the levels of TG,TC,LDL-C and FFA （P〈0.01）,and increased the levels of HDL-C （ P〈0.05,P〈0.01） . The levels of IL-1,IL-6 and TNF-αwere reduced in aqueous extract groups and 50%alcohol high-and middle-dose extract groups （ P〈0.05,P〈0.01） . The expression of TLR4 and p38MAPK mRNA in liver tissue was reduced in aqueous extract groups and 50% alcohol high- and middle-dose extract groups （ P〈0.05,P〈0.01） . Conclusion Abrus mollis Hance plays an anti-inflammatory role and may improve lipid metabolism disorder by regulation of TLR4/p38MAPK pathway.