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[摘要]
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。
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[Abstract]
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.
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