CAJ | 학술논문

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。
목적：본문분석양화응격급세포조망궤제재련뇨좌균소( Streptozotocin,STZ)유도적당뇨병대서백내장발병중적삼여궤제급갈근소적개선작용,위상관연구여림상치료제공차감。 　　방법：SD대서수궤분위사조：대조조、당뇨병모형조、갈근소간예조급을선향초소조。복강주사STZ(65mg/kg)복제당뇨병대서모형,Western Blotting분석각조정상체조직중양화응격급세포조망상관단백표체적변화。 　　결과：당뇨병대서모형복제성공,차대서정상체조직중양화응격단백분자p22、p47급p67표체상조( P<0.05),세포조망단백Bax급Caspase 3표체상조,Bcl2표체하조( P<0.05)。을선향초소화갈근소대상술이상구유현저적개선작용(P<0.05)。 　　결론：NADPH양화매개도적양화응격급P53화Bax/Bcl2개도적세포조망신호통로삼여료당뇨병대서백내장적발병과정,차갈근소통과억제상술양화응격통로기도개선작용。
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.