盐酸维格列汀对非酒精性脂肪肝大鼠肝组织UCP-2的表达及血清炎性因子的影响

Effect of vildagliptin hydrochloride on expression of UCP-2 and serum inflammatory factors in livers of rats with nonalcoholic fatty liver disease

目的:探讨分析盐酸维格列汀对非酒精性脂肪肝大鼠肝组织UCP-2的表达及血清炎性因子的影响。方法:SD大鼠24只,体重120~170 g,平均体重(152.92±10.23)g,随机分为对照组、模型组、干预组。对照组大鼠给予正常饮食结合等量生理盐水皮下注射;模型组大鼠给予正常饮食,并以0.3 mL/10 g给予5%CCl 4花生油溶液皮下多点注射,1次/5d;干预组大鼠在造模后给予盐酸维格列汀50 mg/kg·d,灌胃给药。比较不同组大鼠肝组织病理改变,肝组织UCP-2肝组织表达,血清IL-6、TNF-α水平及肝功能。结果:对照组大鼠的肝组织病理学形态变化正常,且未见UCP2阳性肝细胞;模型组大鼠肝组织病理学形态存在程度不一的变性,且细胞体积出现异常增大,UCP2阳性肝细胞广泛分布,主要分布在细胞浆中与脂肪化程度呈现正相关;干预组大鼠UCP2阳性肝细胞显著减少。对照组P65和探针基本没有结合,模型组结合明显增多,干预组结合能力降低,干预后P65的细胞核转移能力和结合启动下游因子转录的能力降低,差异具有统计学意义(P<0.05);干预组大鼠血清IL-6、TNF-α水平及肝功能指标水平较模型组显著下降,差异具有统计学意义(P<0.05)。结论:盐酸维格列汀可抑制非酒精性脂肪肝大鼠肝组织UCP-2的表达,降低血清IL-6、TNF-α炎性因子水平,促进肝功能恢复,为非酒精性脂肪肝的防治提供新的思路。

Objective:To investigate the effect of vildagliptin hydrochloride on the expression of UCP-2 and serum inflammatory factors in rats with nonalcoholic fatty liver disease.Methods:24 experimental SD rats,weighing 120-170 g,average body weight(152.92±10.23)g,were randomLy divided into the control group,the model group and the intervention group,8 SD rats in each group.The control group were given normal diet and subcutaneous injection of the same amount of normal saline,the model group were given normal diet and 5%CCl 4 peanut oil solution 0.3mL/10g through multi-point subcutaneous injection,1 time/5 days and the intervention group were given intragastric administration of vildagliptin hydrochloride 50mg/kg·d after being modeled,with pathological changes,liver tissue expression of UCP-2,serum IL-6,TNF-αlevels and liver function compared.Results:The pathological changes of liver tissue in the control group were normal,and no UCP2 positive hepatocytes were observed.The pathological morphology of liver tissue in the model group showed different degrees of degeneration.The abnormal volume increased,and UCP2 positive hepatocytes were widely distributed.The main distribution in the cytoplasm was positively correlated with the degree of pimelosis.The UCP2-positive hepatocytes in the intervention group were significantly decreased.In the control group,there was almost no binding between P65 and probes;in the model group,the binding increased significantly;in the intervention group,the binding ability decreased and the ability of P65 to transfer cell nuclei and the ability to initiate transcription of downstream factors decreased after intervention.The difference was statistically significant(P<0.05).The levels of serum IL-6,TNF-αand liver function in the intervention group were significantly higher than those in the model group,the difference being statistically significant(P<0.05).Conclusion:Vildagliptin hydrochloride can inhibit the expression of UCP-2 in liver tissue of rats with nonalcoholic fatty liver disease,reduce the levels of serum IL-6 and TNF-αinflammatory factors,and promote the recovery of liver function,which provides new ideas for prevention of nonalcoholic fatty liver disease.