论文部分内容阅读
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。
Objective: To study the protective effect of palmatine on diabetic aorta and its mechanism. Methods: Thirty-two weeks old db / db mice were randomly divided into diabetic model group, low dose palmatine group [75 mg / (kg · d)] and middle dose group [150 mg / (kg · d) High dose group [300 mg / (kg · d)], and 8 db / m mice as control group. The mice in each group were given gavage for 12 weeks. The diabetic model group and the control group were given the same amount of normal saline. The pathological changes of the aorta in each group were observed by HE staining. The ultrastructure of the aorta in each group was detected by transmission electron microscopy. The fasting blood glucose (FBG) and the levels of total cholesterol Triglyceride); and the serum total antioxidant capacity (T-AOC), malondialdehyde (MDA), reactive oxygen species (ROS) and superoxide dismutase The superoxide dismutase (SOD) levels were detected by Western blot. The expressions of heme oxygenase-1 (HO-1) and nuclear factor E2- related factor 2, Nrf2). Results: The results of HE staining showed that the degree of aortic tissue lesion in mice after palmatine treatment was significantly reduced. The transmission electron microscopy results showed that ultrastructural damage of aortic tissue was relieved in mice treated with palmatine. Compared with diabetic model mice (P = 0.000, P = 0.000); serum MDA and ROS levels were significantly lower (P = 0.000, P = 0.000), while SOD activity and (P = 0.000, P = 0.000). The expressions of Nrf2 and HO-1 in aorta tissue were significantly increased (P = 0.000, P = 0.000), and the differences among different dose groups were 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: Palmatine can effectively protect the aortic tissue of db / db mice. The mechanism may be related to reducing fasting blood glucose and blood lipid levels, activating Nrf2 / HO-1 signaling pathway and relieving oxidative stress in diabetic mice.