缬沙坦对糖尿病大鼠心肌保护作用以及氧化应激的影响  

Effect of Valsartan on Myocardial Protection and Oxidative Stress in Diabetic Rats

作　　者：汪晓霞[1] 王婵媛[1] 林颖慧[1] 武晓碧 张希尧[1] 

机构地区：[1]哈尔滨医科大学附属第四医院内分泌与代谢病科,黑龙江哈尔滨150001

出　　处：《现代生物医学进展》2015年第24期4627-4630,共4页Progress in Modern Biomedicine

基　　金：黑龙江省教育厅(12521196)

摘　　要：目的:探讨缬沙坦对糖尿病大鼠心肌的保护作用及氧化应激影响。方法:以链脲佐菌素建立糖尿病大鼠模型,缬沙坦干预治疗12周后,采用ELISA法检测血清中8脱氧鸟酐(8-OHd G)含量、超氧化物歧化酶(SOD)活性,PCR测定心肌NADPH氧化酶亚型NOX2m RNA、p47phox m RNA表达,采用原位末端标记法(TUNEL)检测心肌细胞凋亡。结果:糖尿病大鼠经缬沙坦干预治疗后,8-OHd G含量,NOX2和p47phox m RNA表达均显著降低(P<0.05),SOD活性升高(P<0.01),心肌细胞凋亡指数显著降低(P<0.05)。结论:高血糖导致糖尿病大鼠氧化应激增强和心肌细胞凋亡增加,缬沙坦可降低糖尿病大鼠氧化应激反应及减少心肌细胞凋亡,因而对心肌有一定的保护作用。Objective： To explore the effects of Valsartan on cardiomyocyte apoptosis and oxidative stress in diabetic rats. Methods：Male mice received streptozotocin to induce diabetes. After 12 weeks of Valsartan treatment, The levels of serum 8-OHd G and activity of SOD were measured by ELISA, the NADPH oxidase subunits NOX2, and p47 phox m RNA expressions in rat myocardium tissues were detected with real-time fluorescence quantitative polymerase chain reaction（PCR）. Apoptosis was evaluated by means of terminal-deoxynucleotidyl transferase mediated d-UTP nick end labeling（TUNEL）. Results： Our results showed significant decrease in the expressions of NOX2 and p47 phox m RNA（P〈0.05）, levels of 8-OHd G（P〈0.01） and the apoptotic index, a marked increase in the activity of SOD（P〈0.01） in cardiac tissues of rats after treatment with Valsartan. Conclusion： High glucose can induce oxidative stress and cardiomyocyte apoptosis, while Valsartan may inhibit oxidative stress and cardiomyocyte apoptosis, thereby plays a protective role in the cardiomypathy of diabetic rats.

关 键 词：糖尿病 心肌 氧化应激 缬沙坦 凋亡 

分 类 号：R587.1[医药卫生—内分泌]