巴马汀对糖尿病小鼠主动脉的保护作用及机制研究

发布时间：2018-04-29 23:08

  本文选题：巴马汀 + 氧化应激　； 参考：《重庆医科大学学报》2017年11期

【摘要】：目的:研究巴马汀对糖尿病小鼠主动脉的保护作用并探讨其机制。方法:8周龄db/db小鼠32只随机分为糖尿病模型组、巴马汀低剂量组[75 mg/(kg·d)]、中剂量组[150 mg/(kg·d)]、高剂量组[300 mg/(kg·d)],并以8只db/m小鼠作为对照组。各组小鼠经灌胃给药12周,糖尿病模型组和对照组小鼠给予等量的生理盐水。通过HE染色观察各组小鼠主动脉组织病理变化情况;通过透射电镜检测各组小鼠主动脉超微结构变化;检测各组小鼠空腹血糖(fasting blood glucose,FBG)和血脂(总胆固醇和甘油三脂);并检测各组小鼠血清中总抗氧化力(total antioxidant capacity,T-AOC)、丙二醛(malondialdehyde,MDA)、活性氧(reactive oxygen species,ROS)和超氧化物歧化酶(superoxide dismutase,SOD)的水平;通过Western blot检测各组小鼠主动脉组织中血红素加氧酶1(heme oxygenase-1,HO-1)和核因子E2相关因子2(nuclear factor E2-related factor 2,Nrf2)的表达。结果:HE染色结果表明巴马汀治疗后的小鼠主动脉组织病变程度明显降低;透射电镜结果表明巴马汀治疗后的小鼠主动脉组织超微结构损伤显著减轻;与糖尿病模型组小鼠相比,巴马汀治疗后的小鼠空腹血糖和血脂均显著降低(P=0.000,P=0.000);血清MDA和ROS水平均明显降低(P=0.000,P=0.000),而SOD活性和T-AOC则均显著增强(P=0.000,P=0.000),主动脉组织中Nrf2和HO-1蛋白的表达水平明显提高(P=0.000,P=0.000),并且各剂量组间差异均显著(P=0.000,P=0.000,P=0.000,P=0.000,P=0.000,P=0.000,P=0.000,P=0.000)。结论:巴马汀可以有效保护db/db小鼠主动脉组织,其机制可能与降低糖尿病小鼠的空腹血糖和血脂含量,激活Nrf2/HO-1信号通路并减轻氧化应激反应有关。
[Abstract]:Objective: To study the protective effect of Bamatin on the aorta of diabetic mice and explore its mechanism. Methods: 32 db/db mice of 8 weeks old were randomly divided into diabetic model group, [75 mg/ (kg. D) in low dose group of Ba, [150 mg/ (kg d) in medium dose group, [300 mg/ in high dose group (kg.)), and 8 mice as control group. After 12 weeks, the diabetic model group and the control group were given the same amount of normal saline. The pathological changes of aortic tissue were observed by HE staining, and the ultrastructural changes of aorta in each group were detected by transmission electron microscope, and the blood glucose (fasting blood glucose, FBG) and blood lipid (total cholesterol and glycerol three fat) were detected in each group. The total antioxidant capacity (total antioxidant capacity, T-AOC), malondialdehyde (malondialdehyde, MDA), reactive oxygen species (reactive oxygen species, ROS) and superoxide dismutase (superoxide dismutase) were detected in all groups of mice, and the heme oxygenase 1 in the aorta tissues of all mice was detected. HO-1) and the expression of nuclear factor E2 related factor 2 (nuclear factor E2-related factor 2, Nrf2). Results: the results of HE staining showed that the degree of pathological changes in the aorta tissue of mice after the treatment of Martin was obviously reduced; the transmission electron microscope results showed that the ultrastructural damage of the aorta group in the mice after the treatment of BA was significantly reduced; and that of the diabetic model group was smaller. In mice, the fasting blood glucose and blood lipid decreased significantly (P=0.000, P=0.000), and the levels of serum MDA and ROS were significantly decreased (P=0.000, P=0.000), while SOD activity and T-AOC were significantly enhanced (P=0.000, P=0.000), and the expression level of Nrf2 and HO-1 protein in the aorta was significantly increased, and the dose groups were in each dose group. The difference was significant (P=0.000, P=0.000, P=0.000, P=0.000, P=0.000, P=0.000, P=0.000, P=0.000). Conclusion: Martin can effectively protect the aorta of db/db mice. The mechanism may be related to reducing the fasting blood glucose and blood lipid content in diabetic mice, activating the Nrf2/HO-1 signaling pathway and alleviating the oxidative stress response.

【作者单位】： 第三军医大学新桥医院中医科;第三军医大学大坪医院外研所;第三军医大学新桥医院中心实验室;
【分类号】：R587.2
，

本文编号：1821973