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 endoplasmic reticulum stress proteins were detected by Western Blotting. Results The ± dp/ dtmax in diabetic rats increased while the ex-pression of p22phox,p47phox,PERK,CHOP as well as Bax increased accompanying Bcl2 decrease. DPI medication alleviated these abnormali-ties greatly. Conclusion NADPH oxidase mediated endoplasmic reticulum stress is involved in STZ induced diabetic cardiomyopathy and DPI can alleviate by inhibiting NADPH oxidase.
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