糖尿病大鼠心肌病的NADPH氧化酶介导内质网应激机制研究及DPI的改善作用

NADPH oxidase mediated endoplasmic reticulum stress is involved in diabetic cardiomyopathy and the alleviations of DPI

目的本研究探讨糖尿病心肌病的NADPH氧化酶介导内质网应激机制研究及二甲苯基碘(DPI)的改善作用。方法 SD大鼠随机分为三组:对照组、糖尿病组和DPI治疗组(n=8)。腹腔注射链脲佐菌素(65 mg/kg)复制糖尿病心肌病模型,Western Blotting分析大鼠左心室NADPH氧化酶亚基及内质网应激蛋白的表达变化。结果糖尿病组大鼠左心室±dp/dtmax明显增高,p22phox、p47phox及PERK、CHOP表达明显增强,而DPI干预组上述表达异常得到显著的恢复。结论 NADPH氧化酶介导的内质网应激是糖尿病心肌病发病的重要机制,DPI具有显著改善糖尿病心肌病的作用。

Objective The present research aimed to explore the involvement of endoplasmic reticulum stress in diabetic cardiomyopathy. Methods SD rats were divided into 3 groups, control group, diabetic group and DPI intervention group. Diabetic rats were duplicated by injec- tion of STZ （65 mg/kg） and DPI group received DPI treatment in the lase 28 d. The expression of p22phox, p47phox, p67phox, gp91phox as well as cndoplasmic reticulum stress proteins were detected by Western Blotting. Results The ＋ dp/dtmax in diabetic rats increased while the expression of p22phox, p47phox, PERK, CHOP as well as Bax increased accompanying Bcl2 decrease. DPI medication alleviated these abnormalities greatly. Conclusion NADPH oxidase mediated endoplasmic reticulum stress is involved in STZ induced diabetic cardiomyopathy and DPI can alleviate by inhibiting NADPH oxidase.