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ID:17712892
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时间:2018-09-05
《姜黄素对单侧输尿管梗阻后肾间质纤维化的调节.doc》由会员上传分享,免费在线阅读,更多相关内容在学术论文-天天文库。
1、姜黄素对单侧输尿管梗阻后肾间质纤维化的调节作者:张彬王全胜朱锐汪永辉张丽晓徐敏刘建国【摘要】目的:研究姜黄素在单侧输尿管梗阻(UUO)大鼠模型中能否减少肾间质中转化生长因子β1(transforminggrowthfactor-β1,TGF-β1)和结缔组织生长因子(connectivetissuegrowthfactor,CTGF)的表达。方法:将30只大鼠随机分为3组,每组10只:假手术组、模型组、姜黄素组。模型组和姜黄素组行右侧输尿管接扎术,假手术组只游离不接扎。术后第14天处死各组中的大鼠,检测血液尿素氮(BUN)、血清肌酸酐(Scr)。用免疫组织化学方法测定TGF-β1、
2、CTGF的表达情况,同时采用Masson染色,观察肾脏病理情况。结果:姜黄素降低了BUN、Scr的含量,同时姜黄素显著减少了大鼠肾间质TGF-β1、CTGF的表达,并有效改善了肾脏的病理学损伤。结论:姜黄素可以减少输尿管梗阻后TGF-β1、CTGF的表达,从而改善UUO所致的肾脏损伤,提示姜黄素可能有延缓慢性肾脏疾病纤维化进程的潜能。【关键词】输尿管梗阻;纤维化;姜黄素;免疫组织化学;大鼠,Spragua-Dawley;肾间质[Abstract]Objective:Toverifyifcurcumincandecreasetheexpressionoftransforminggro
3、wthfactor-β1(TGF-β1)andconnectivetissuegrowthfactor(CTGF)inunilateralureteralobstruction(UUO)ratmodelsduringtheprocessofrenalinterstitialfibrosiscausedbyunilateralureteralobstruction(UUO).Methods:TheexperimentwassuccessfullyconductedfromMaytoAugust,2007inUnionHospitalAffiliatedtoTongjiMedicalC
4、ollegeofHuazhongUniversityofScienceandTechnology.ThirtySprague-Dawleyratswererandomlydividedintothreegroups:shamoperatedgroup,UUOmodelgroup,andcurcumin-treatedgroup(10ineachgroup).TheratsintheUUOmodelgroupandcurcumin-treatedgroupunderwentUUOsurgery.Ratsincurcumin-treatedgroupweregivenwatersusp
5、ensionofcurcuminpowder(200mg·kg-1·d-1)orally,whilethoseinUUOmodelgroupandshamoperationgroupweregivenwateronlyinstead.Alloftheratswerekilledin14daysaftersurgery.Thelevelsofbloodureanitrogen(BUN)andserumcreatinine(Scr)weremeasured,histologicalchangeswereobservedwithMassonstainmethod,andImmunohis
6、tochemistrywasperformedonrenaltissuetodetectTGF-β1andCTGF.Results:Intheobstructedkidneys,thereweresignificantrenalinterstieialfibrosisandinterstitialspaceexpansion.ImmunohistochemicalstainingshowedthattheexpressionofTGFβ1andCTGFwassignificantlyincreasedintheobstructedkidneys.Incomparisonwithth
7、emodelgroup,BUNandScrlevels,interstitial5volume,andtheexpressionofTGF-β1andCTGFincurcumin-treatedgroupweresignificantlydecreased.Conclusions:Theresultsindicatethatcurcumincandown-regulatetheexpressionofTGF-β1andCTGFinUUOrats,throughwhic
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