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作 者:禹刚 刘修恒[1] 王磊[1] 陈晖[1] 陈志远[1] 邱涛[1] 翁小东[1] 贾海飞 何力[1] 曾光[1]
机构地区:[1]武汉大学人民医院泌尿外科,湖北武汉430060
出 处:《武汉大学学报(医学版)》2015年第3期337-340,共4页Medical Journal of Wuhan University
基 金:湖北省自然科学基金资助项目(编号:2013CFB226)
摘 要:目的:探讨臭氧预处理对大鼠肾脏缺血-再灌注损伤后纤维化是否具有保护作用及其相关机制。方法:取24只雄性Wistar大鼠,按随机数字法分为3组,每组8只:假手术组(Sham组):麻醉后游离双侧肾脏,切除大鼠右肾,缝合腹壁;缺血-再灌注组(IRI组):麻醉后游离双侧肾脏,切除右肾,在左肾游离之后夹闭左肾动、静脉45min,然后开放再灌注8周;臭氧预处理组(OzoneOP组):术前15d对该组大鼠经直肠吹入氧气和臭氧的混合气体5.0-5.5ml[臭氧浓度为50mg/L,1.0mg/(kg·d],其余手术操作与缺血-再灌注组相同。测定大鼠肾功能指标血清肌酐(Cr)和尿素氮(BUN),HE染色观察大鼠肾组织病理变化,Realtime PCR和Western blot测定大鼠肾组织标本中α-SMA、TGF-β1和Smad7的表达水平。结果:3组大鼠肾功能指标无明显统计学差异(P>0.05);光镜下,假手术组大鼠肾组织结构近似正常,臭氧预处理组及缺血-再灌注组肾组织结构可见破坏,臭氧预处理组肾组织破坏程度明显轻于缺血-再灌注组;Western blot和Realtime PCR结果显示:与假手术组相比,缺血-再灌注组的α-SMA、TGF-β1表达水平明显增高(P<0.05),而Smad-7的表达水平明显降低(P<0.05)。臭氧预处理组与缺血-再灌注组相比,α-SMA、TGF-β1水平明显降低(P<0.05),而Smad-7的表达水平明显增高(P<0.05)。结论:臭氧预处理对大鼠肾脏缺血-再灌注后纤维化有保护作用,其机制可能与影响TGF-β1、Smad7等的表达有关。Objective:To investigate the protective effect of ozone preconditioning on renal fibrosis after ischemia-reperfusion injury in rat and its mechanisms.Methods:Twenty-four male Wistar rats were randomly divided into 3groups as sham operation group,ischemia-reperfusion group,and ozone preconditioning group.Renal and serum samples were collected.The concentration of serum creatinine and blood urea were detected 8weeks later.And after HE staining,the pathological changes in the left kidneys of rats were observed under the light microscope.The expressions ofα-SMA,TGF-β1and Smad7 were detected by Realtime PCR and Western blot.Results:There was no statistical difference in the renal function among the three groups(P〈0.05);More renal damages could be observed in the ischemia-reperfusion group than in the ozone pre-treatmentgroup.Ozone preconditioning could obviously alleviate the renal injury induced by ischemia and reperfusion injury.The test results of Western blot and Realtime PCR showed that the expressions ofα-SMA and TGF-β1were higher in the ischemia-reperfusion group than in the ozone preconditioning group(P〈0.05).And the expression of Smad-7was higher in the ozone preconditioning group than in the ischemia-reperfusion group(P〈0.05).Conclusion:The ozone preconditioning is the protective factor to the renal fibrosis after ischemia reperfusion injury in rat,and its mechanism is possibly related to the expressions of TGF-β1and Smad 7.
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