锦南复方对2型糖尿病大鼠血糖的辅助调节作用

Auxiliary Effect of Jinnan Compound on the Regulation of Blood Glucose in Type 2 Diabetic Rats

摘要:

本研究探讨了锦南复方对2型糖尿病大鼠的降糖作用。随机选取10只SD大鼠作为正常对照组，剩余40只采用高脂饮食喂养联合低剂量链脲佐菌素诱导2型糖尿病模型。将成模大鼠随机分为3组：模型组、阳性对照组（二甲双胍，200 mg/kg）、锦南复方组（锦南复方，500 mg/kg）。干预7周后，检测大鼠血糖、血脂、胰岛β细胞中γ-氨基丁酸（γ-aminobutyric acid，GABA）表达水平、Bax蛋白水平，RT-PCR检测肝脏中PPAR-α、PPAR-γ基因表达。电子扫描显微镜观察大鼠腹主动脉血管壁变化。结果表明，锦南复方组大鼠空腹血糖、餐后血糖、糖化血红蛋白、血清胰岛素、甘油三酯、总胆固醇、低密度脂蛋白、Bax蛋白相对表达量分别为18.45 mmol/L、21.39 mmol/L、8.97%、26.78 mIU/L、3.35 mmol/L、2.53 mmol/L、0.46 mmol/L、0.20，均显著低于模型组（p<0.01）；GABA、PPAR-α、PPAR-γ相对表达量为0.36、0.79、4.42，均显著高于模型组(p<0.05)。锦南复方组大鼠血管内壁损伤程度低于模型组。推测降糖作用机制可能与增加胰岛GABA表达，启动PI3K/PKB通路，抑制胰岛β细胞凋亡，上调PPAR-α、PPAR-γ基因表达，加速肝脏脂肪酸的β氧化，减少脂肪酸含量有关。

Abstract:

This study explored the hypoglycemic effect of Jinnan compound on type 2 diabetes in a rat model. Ten SD rats were randomly selected as the normal control group, and the remaining 40 rats were fed a high-fat diet combined with a low-dose streptozotocin and established type 2 diabetes model rats. The type 2 diabetes model rats were randomly divided into three groups: model group, positive group (metformin, 200 mg/kg) and Jinnan compound treatment group (Jinnan compound, 500 mg/kg). After 7 weeks of intervention, the levels of blood sugar and lipids, and the expression levels of γ-aminobutyric acid (GABA) and Bax protein in islet β cells were determined, while the expression of PPAR-α and PPAR-γ genes were detected by RT-PCR. Electron scanning microscopy was used to examine the changes in aortic walls of abdominal rats. The results showed that the levels of fasting blood sugar (18.45 mmol/L), postprandial glucose (21.39 mmol/L), glycosylated hemoglobin (8.97%), insulin (26.78 mIU/L), triglyceride (3.35 mmol/L), total cholesterol (2.53 mmol/L), low-density lipoprotein (0.46 mmol/L) and relative expression of Bax (0.2) in the Jinnan compound treatment group significantly decreased, whilst the relative expression levels of GABA (0.36), PPAR-α (0.79) and PPAR-γ (4.42) in the Jinnan compound treatment group increased markedly (p<0.05), compared with those of the model group (p <0.01). The extent of injury in the Jinnan compound treatment group was lower than that of the model group. It is speculated that the mechanism underlying the hypoglycemic action of Jinnan compound might be related to the increase of islet GABA expression, activation of PI3K/PKB signal pathway, inhibition of islet β cell apoptosis, up-regulation of the expression of PPAR-α and PPAR-γ genes, acceleration of β-oxidation of liver fatty acids, and decrease of fatty acid content.