论文部分内容阅读
目的探讨糖尿病大鼠心肌组织内脏脂肪素(Visfatin)、磷脂酰肌醇酶-3激酶(PI3K)表达及二甲双胍对其干预的作用。方法 60只SD大鼠随机分为正常对照(NC)组、糖尿病(DM)组、二甲双胍治疗(M+DM)组,成模后测定FBG、FIns、FFA、TG、TC、LDL-C,计算胰岛素抵抗指数(HOMA-IR)、ISI;测定心肌Visfatin、PI3K mRNA表达及Visfatin蛋白表达;观察心肌病理变化。结果 DM组FBG、FFA、TG、TC、FIns、HOMA-IR较NC组增高(P<0.05),M+DM组较DM组降低(P<0.05)。DM组心肌组织Visfatin、PI3K mRNA表达较NC组降低(P<0.05),M+DM组心肌组织Visfatin、PI3KmRNA表达均较DM组增高(P<0.05);M+DM组心肌组织Visfatin蛋白表达较DM组增高(P<0.05)。结论二甲双胍可提高糖尿病大鼠心肌组织Visfatin、PI3K表达,对心肌组织保护的作用机制可能是通过调节心肌Visfatin表达水平进而通过PI3K途径完成。
Objective To investigate the expression of visfatin and phosphatidylinositol 3 - kinase (PI3K) in myocardium of diabetic rats and the effect of metformin on it. Methods Sixty Sprague-Dawley rats were randomly divided into normal control (NC), diabetic (DM) and metformin-treated (M + DM) groups. FBG, FIns, FFA, TG, TC and LDL- Insulin resistance index (HOMA-IR), ISI; Visfatin, PI3K mRNA expression and Visfatin protein expression were measured; myocardial pathological changes were observed. Results The levels of FBG, FFA, TG, TC, FIns and HOMA-IR in DM group were higher than those in NC group (P <0.05), and those in M + DM group were lower than those in DM group (P <0.05). The visfatin and PI3K mRNA expressions in myocardium of DM group were significantly lower than those of NC group (P <0.05), while the levels of Visfatin and PI3K mRNA in DM group were higher than that of DM group (P <0.05) DM group increased (P <0.05). Conclusion Metformin can increase the expression of Visfatin and PI3K in myocardium of diabetic rats. The mechanism of myocardial protection may be through the regulation of Visfatin expression in myocardium and PI3K pathway.