祛湿活血方对非酒精性脂肪性肝病大鼠血清肿瘤坏死因子-α和脂联素的调节

Effect of Qushi Huoxue decoction on serum TNF-α and adiponectin in NAFLD rats

目的:通过研究祛湿活血方对非酒精性脂肪性肝病(NAFLD)模型大鼠血清肿瘤坏死因子-α(TNF-α)和脂联素表达的影响,探讨祛湿活血方防治NAFLD的可能机制。方法:采用高脂高糖饲料建立SD大鼠NAFLD模型,后用祛湿活血方(成人50kg计算的10倍剂量)进行干预性治疗8周,并用正常饮食组、高脂模型组、维生素E(40mg/kg-1.d-1)组、牛磺熊去氧胆酸(75mg/kg-1.d-1)组以及吡格列酮(3mg/kg-1.d-1)组大鼠做对照。用ELISA法检测大鼠血清TNF-α和脂联素。结果:高脂模型组大鼠较正常饮食组TNF-α明显增高,而脂联素明显降低(P均<0.05),不同干预方案中,尽管祛湿活血方、维生素E以及吡格列酮均可不同程度降低血清TNF-α水平,但与高脂模型组比较差异无显著性意义。祛湿活血方可明显升高脂联素水平,与正常饮食组水平相当(P>0.05),与高脂模型组比较,差异有显著性意义(P<0.01);维生素E、牛磺熊去氧胆酸以及吡格列酮组大鼠脂联素水平与高脂模型组比较,差异无显著性意义(P>0.05)。结论:祛湿活血方对NAFLD的防治作用,可能不是通过对TNF-α的调节,而是通过对脂联素表达的调节而实现。

Objective： To study the effect of Qushi Huoxue decoction on serum levels of tumor necrosis factor alpha （TNF- alpha） and adiponeetin in rats model of non-alcoholic fatty liver disease （NAFLD） and to further explore the possible mechanism of Qushi Huoxne decoction in prevention and treatment of NAFLD. Methods： After made NAFLD model by raising SD rats with high-fat and high-sugar diet, Qushi Huoxue decoction treated NAFLD rats for 8 weeks, and normal diet group, NAFLD model group, vitamin E （40mg/kg -1 d -1 ）, tauroeholic ursodeoxycholic acid （ 75mg/kg - 1 d -1 ）, and pioglitazone （ 3mg/kg -1 . d-1 ） were used as control groups. Serum levels of TNF-ct and adiponectin were measured by ELISA. Results： TNF-α was in- creased significantly in the model group than the normal diet group, while adiponectin was reduced significantly （ P 〈 0. 05 ） in the different medicine groups. Despite Qushi Huoxue decoction, vitamin E and pioglitazone can be reduced serum TNF-αlevel, but there were no significant difference contrasting with NAFLD model group. The adiponectin levels was higher in Qushi Huoxue decoction group than NAFLD model group （P 〈0. 01 ）, and reached the normal diet group level （P 〉 0. 05） . The level of adi- ponectin was no difference between high-fat diet group and vitamin E, the taurocholic ursodeoxycholic acid and pioglitazone groups （P 〉 0.05） . Conclusion： The Qushi Huoxue decoction may be not through the regulation of TNF-α but through the regulation of adiponectin in the prevention and treatment of NAFLD.