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作 者:王晓松[1] 成秀梅[1] 曹焕敏[1] 姚晓光[1] 刘斌[1]
机构地区:[1]河北医科大学中西医结合学院,河北石家庄050091
出 处:《吉林大学学报(医学版)》2011年第3期479-482,I0004,共5页Journal of Jilin University:Medicine Edition
基 金:河北省教育厅科技攻关计划资助课题(2007439)
摘 要:目的:观察糖尿病肾病模型大鼠血浆一氧化碳(CO)的变化和血红素氧合酶-1(HO-1)、血红素氧合酶-2(HO-2)在肾脏组织的表达,探讨血红素氧合酶/一氧化碳(HO/CO)系统在糖尿病肾病发生和发展中的作用。方法:将24只SD大鼠随机分为对照组和模型组,按Anderson等方法建立糖尿病肾病模型。8周后收集尿液测定24 h的尿蛋白(Upro)和尿肌酐(Ucr);大鼠断头取血测定CO、尿素氮(BUN)和肌酐(Scr),计算肌酐清除值(Ccr);剖取肾脏组织,采用免疫组织化学法检测肾脏组织HO-1和HO-2的表达。结果:与对照组比较,模型组大鼠Upro、BUN和Scr明显升高(P<0.01),Ccr降低(P<0.01);模型组大鼠血浆CO与对照组比较明显降低(P<0.01),肾脏组织HO-1和HO-2的表达强度显著减弱(P<0.01)。结论:HO/CO的调节失常参与了糖尿病肾病的发生和发展。Objective To observe the change of plasma carbon monoxide(CO) and the expressions of heme oxygenase-1(HO-1) and heme oxygenase-2(HO-2) in kidney tissues,and explore the effect of heme oxygenase/carbon monoxide(HO/CO)on development and progression of diabetic nephropathy.Methods 24 Sprague-Dawley rats were randomly divided into control group and model group,The rat models with diabetic nephropathy were established according to Anderson' method.8 weeks later,the urine of rats were collected to measure the 24 h urinary protein(Upro)and urinary creatinine(Ucr);the rats were sacrificed to measure the levels of CO,blood urea nitrogen(BUN),serum creatinine(Scr),meanwhile the Ccr was calculated;the kidneys were harvested for observing the expressions of HO-1 and HO-2 by immunohistochemistry.Results The contents of Upro,BUN and Scr all were increased in model group,but Ccr and CO were decreased compared with control group(P0.01);the content of plasma CO in model group was obviously lower than that in control group(P0.01);the expressions of HO-1 and HO-2 in kidney tissues were obviously reduced compared with control group(P0.01).Conclusion The abnormal regulation of HO/CO is involved in the development and progression of diabetic nephropathy.
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