链脲佐菌素诱导糖尿病性大鼠白内障的氧化应激-细胞凋亡机制及葛根素的改善作用

Oxidative stress-apoptosis mediated STZ-induced diabetic cataract and the interventions of puerarin

目的:本文分析氧化应激及细胞凋亡机制在链脲佐菌素(Streptozotocin,STZ)诱导的糖尿病大鼠白内障发病中的参与机制及葛根素的改善作用,为相关研究与临床治疗提供借鉴。方法:SD大鼠随机分为四组:对照组、糖尿病模型组、葛根素干预组及乙酰香草素组。腹腔注射STZ(65mg/kg)复制糖尿病大鼠模型,Western Blotting分析各组晶状体组织中氧化应激及细胞凋亡相关蛋白表达的变化。结果:糖尿病大鼠模型复制成功,且大鼠晶状体组织中氧化应激蛋白分子p22、p47及p67表达上调(P<0.05),细胞凋亡蛋白Bax及Caspase 3表达上调,Bcl2表达下调(P<0.05)。乙酰香草素和葛根素对上述异常具有显著的改善作用(P<0.05)。结论:NADPH氧化酶介导的氧化应激及P53和Bax/Bcl2介导的细胞凋亡信号通路参与了糖尿病大鼠白内障的发病过程,且葛根素通过抑制上述氧化应激通路起到改善作用。

AIM：To explore the involvement of oxidative stress and apoptosis in the pathogenesis of diabetic cataract induced by Streptozotocin （ STZ） and the interventions of puerarin in order to supply references for clinical treatment. METHODS：Male SD rats were divided into four groups randomly, control group, diabetic group, apocynin group and puerarin group. The diabetic group were replicated by single injection of STZ （65mg/kg, ip）. The expression of p22, p47, p67, Bax/Bcl2, Caspase 3 and P53 proteins were detected by Western Blotting. RESULTS：The diabetic rats were replicated successfully and the expression of Bcl2 was downregulated while the expression of p22, p47, p67, Bax, Caspase 3 and P53 were upregulated in diabetic group with a significant statistical differences when compared with control group （P〈0. 05）. Apocynin and prerarin can reverse the abnormal expression of the aforementioned proteins dramatically （P〈0. 05）. CONCLUSION： NADPH oxidase mediated oxidative stress and P53, Bax/Bcl2 mediated apoptosis are involved in the pathogenesis of diabetic cataract and puerarin can alleviate cataract greatly by inhibiting the aforementioned signal pathway.