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作 者:陈振宇[1] 文艺[1] 张少华[1] 冯犁[1] 闫洪涛[1] 陈光宇[1] 邹洪[1] 汤礼军[1]
机构地区:[1]成都军区成都总医院全军普通外科中心,成都610083
出 处:《世界科技研究与发展》2014年第2期150-154,共5页World Sci-Tech R&D
基 金:全军临床高新技术重大项目(2010g×js040)资助
摘 要:目的观察胃转流术对2型糖尿病大鼠肾脏氧化应激及蛋白激酶C(PKC)活性的影响。方法40只SD大鼠随机分为正常对照组(8只),糖尿病模型组(32只),模型组注射STZ(35 mg/kg),血糖稳定后确定成模30只,再将其分为糖尿病对照组(8只),假手术组(8只),手术组(14只)。术后8周检测各组大鼠空腹血糖、肾重指数(肾重/体重)、尿素氮(BuN)、血肌酐(Cr),测定各组大鼠肾组织总超氧化物歧化酶(TSOD)、谷胱甘肽过氧化酶(GSHPX)活性,脂质过氧化代谢产物丙二醛(MDA)含量及PKC的活性,HE染色观察肾组织病理变化。结果与糖尿病对照组和假手术组相比,手术组能明显降低空腹血糖、改善肾重指数、BUN、Cr等指标(P<0.05),同时肾组织抗氧化酶TSOD、GSH-PX活性增强,MDA含量减少,肾脏PKC活性降低(P<O.05)。HE染色显示手术组病变也明显轻于糖尿病对照组和假手术组。结论胃转流术可能通过抑制2型糖尿病大鼠肾脏氧化应激及PKC活性增强发挥肾脏保护作用。Objective To observe the influence of gastric bypass on renal oxidative stress and the activity of protein kinase C in type 2 diabetic rats. Methods Forty SD rats were randomly divided into normal control group ( n = 8), diabetes model group( n--32), the diabetes model group were injected STZ(35mg/kg) ,when the blood glucose steady, there were 30 rats were considered as the successful diabetes model. Then they were randomly divided into diabetes control group( n = 8 ), dia- betes sham operation group( n = 8 ) and diabetes operation group( n = 14 ) . the kidney hypertrophy index( kidney weight/ body weight, KW/BW), fasting blood glucose ( FBG), blood urea nitrogen ( BUN), serum creatinine ( Cr ), the activities of to- tal superoxide dismutase ( TSOD ), glutathione peroxidase (GSH-PX) and protein kinase C ( PKC ), content of malondialde- hyde ( MDA ) in renal tissue were measured after operation for 8 weeks. In addition, the renal tissue was observed by light mi- croscopy. Results In diabetes operation group, kidney hypertrophy index, FBG, BUN, Cr, content of MDA and the activity of PKC markedly decreased ( P 〈 0.05 ), the activities of TSOD and GSH-PX increased ( P 〈 0. 05 ) compared with diabetes con- trol group and diabetes sham operation group. Renal pathologic changes in diabetes operation group were also improved. Conclusion The gastric bypass could protect the kidney of type 2 diabetic rats, which may be ascribed to the inhibitory effect of oxidative stress and the activity of PKC in renal tissue.
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