本文選題：巴馬汀 + 氧化應(yīng)激�。� 參考：《重慶醫(yī)科大學(xué)學(xué)報(bào)》2017年11期

【摘要】：目的:研究巴馬汀對(duì)糖尿病小鼠主動(dòng)脈的保護(hù)作用并探討其機(jī)制。方法:8周齡db/db小鼠32只隨機(jī)分為糖尿病模型組、巴馬汀低劑量組[75 mg/(kg·d)]、中劑量組[150 mg/(kg·d)]、高劑量組[300 mg/(kg·d)],并以8只db/m小鼠作為對(duì)照組。各組小鼠經(jīng)灌胃給藥12周,糖尿病模型組和對(duì)照組小鼠給予等量的生理鹽水。通過(guò)HE染色觀察各組小鼠主動(dòng)脈組織病理變化情況;通過(guò)透射電鏡檢測(cè)各組小鼠主動(dòng)脈超微結(jié)構(gòu)變化;檢測(cè)各組小鼠空腹血糖(fasting blood glucose,FBG)和血脂(總膽固醇和甘油三脂);并檢測(cè)各組小鼠血清中總抗氧化力(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;通過(guò)Western blot檢測(cè)各組小鼠主動(dòng)脈組織中血紅素加氧酶1(heme oxygenase-1,HO-1)和核因子E2相關(guān)因子2(nuclear factor E2-related factor 2,Nrf2)的表達(dá)。結(jié)果:HE染色結(jié)果表明巴馬汀治療后的小鼠主動(dòng)脈組織病變程度明顯降低;透射電鏡結(jié)果表明巴馬汀治療后的小鼠主動(dòng)脈組織超微結(jié)構(gòu)損傷顯著減輕;與糖尿病模型組小鼠相比,巴馬汀治療后的小鼠空腹血糖和血脂均顯著降低(P=0.000,P=0.000);血清MDA和ROS水平均明顯降低(P=0.000,P=0.000),而SOD活性和T-AOC則均顯著增強(qiáng)(P=0.000,P=0.000),主動(dòng)脈組織中Nrf2和HO-1蛋白的表達(dá)水平明顯提高(P=0.000,P=0.000),并且各劑量組間差異均顯著(P=0.000,P=0.000,P=0.000,P=0.000,P=0.000,P=0.000,P=0.000,P=0.000)。結(jié)論:巴馬汀可以有效保護(hù)db/db小鼠主動(dòng)脈組織,其機(jī)制可能與降低糖尿病小鼠的空腹血糖和血脂含量,激活Nrf2/HO-1信號(hào)通路并減輕氧化應(yīng)激反應(yīng)有關(guān)。
[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.

【作者單位】： 第三軍醫(yī)大學(xué)新橋醫(yī)院中醫(yī)科;第三軍醫(yī)大學(xué)大坪醫(yī)院外研所;第三軍醫(yī)大學(xué)新橋醫(yī)院中心實(shí)驗(yàn)室;
【分類(lèi)號(hào)】：R587.2
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本文編號(hào)：1821973