论文部分内容阅读
目的建立糖尿病小鼠模型,研究硫辛酸(LA)干预后氧化还原状态、糖代谢酶活性和大血管的变化。方法小鼠分为正常对照(NC)组、糖尿病(DM)组和硫辛酸干预(LA)组,每组各10只,检测FBG、FIns,谷胱甘肽还原型氧化型比值(GSH/GSSG),超氧化物歧化酶活性抑制率(SODI),肝脏丙酮酸羧化酶(PC)和己糖激酶(HK)活性;HE染色观察胰岛细胞、电镜观察腹主动脉的微结构。结果 LA组干预6周后,FBG低于DM组[(10.05±0.40)vs(7.03±0.26)mmol/L,P<0.05)];干预结束后GSH/GSSG、肝脏PC活性低于DM组[(23.15×10~(-2)±7.99×10~(-2))vs(36.20×10~(-2)±1.14×10~(-2)),(2.87×10~(-2)±0.32×10~(-2))vs(17.30×10~(-2)±4.01×10~(-2))Abs/μg pro/min,P<0.05];胰岛细胞体积和排列、腹主动脉内皮细胞形态等较DM组恢复。结论 LA可以改善糖尿病小鼠模型氧化应激状态,减轻胰岛细胞和主动脉内皮的损伤。
Objective To establish diabetic mouse model to study the redox status, the activity of glucose metabolism enzymes and the changes of macrovessels after the intervention of lipoic acid (LA). Methods The mice were randomly divided into normal control (NC) group, diabetic (DM) and lipoic acid intervention (LA) groups, with 10 mice in each group. FBG, FIns, GSH / GSSG ), Superoxide dismutase (SODI) activity, hepatic pyruvate carboxylase (PC) and hexokinase (HK) activity. The islet cells were observed by HE staining and the microstructure of abdominal aorta was observed by electron microscope. Results Compared with DM group, FBG in LA group was significantly lower than that in DM group [(10.05 ± 0.40) vs (7.03 ± 0.26) mmol / L, P <0.05). After intervention, the activity of GSH / (23.15 × 10 -2 ± 7.99 × 10 -2) vs (36.20 × 10 -2 ± 1.14 × 10 -2), (2.87 × 10 -2 ± 0.32 × 10 -2 vs 17.30 × 10 -2 ± 4.01 × 10 -2 Abs / μg pro / min, P <0.05]; islet cell volume and arrangement, abdominal aorta Endothelial cell morphology than the DM group recovery. Conclusion LA can improve oxidative stress in diabetic mice and alleviate the damage of islet cells and aortic endothelium.