国际泌尿系统杂志
國際泌尿繫統雜誌
국제비뇨계통잡지
INTERNATIONAL JOURNAL OF UROLOGY AND NEPHROLOGY
2011年
6期
738-741
,共4页
高雁鸿%褚宇东%周晓霜%李荣山
高雁鴻%褚宇東%週曉霜%李榮山
고안홍%저우동%주효상%리영산
肾%再灌注损伤%大鼠
腎%再灌註損傷%大鼠
신%재관주손상%대서
Kidney%Reperfusion Injury%Rats
目的 观察Intermedin(IMD)预处理大鼠肾脏缺血再灌注损伤(IRI)修复过程中细胞周期蛋白E(cyclinE)和其依赖性激酶2(CDK2)表达的变化,IMD可能的促进肾组织再生修复的作用机制.方法 健康雄性Wistar大鼠,体重180~220g,共144只随机分为对照组、IRI组、转空质粒组、转IMD组.对照组和IRI组切除右肾;转空质粒组、转IMD组大鼠切除右肾后,在六氟化硫微泡(声诺维)介导下将空质粒及IMD质粒转染入左肾;1周后分别制作肾脏IRI模型.每组于再灌注1d、2d、3d、4d、7d、14d时各取6只留取肾组织标本.检测各组肾组织中cyclinE与CDK2的表达.结果 IRI组cyclin E、CDK2于再灌注后1d、2d、3d、4d、7d表达逐渐增高,7d时到达最高峰,此后表达逐渐降低,14d时降至最低,但仍有少量表达,与对照组比较差异具有统计学意义(p<0.05).转IMD组各项指标在第1d即开始显著增高,第2d、3d、4d、7d呈进行性下降,至14d时恢复正常,与IRI组相比其差异具有统计学意义(p<0.05);转空质粒组与IRI组以上指标差异无统计学意义.结论 IMD预处理大鼠肾脏缺血再灌注损伤后早期,cyclinE、CDK2的表达明显上调,提示IMD可能通过促进细胞周期进展从而加快肾组织再生修复.
目的 觀察Intermedin(IMD)預處理大鼠腎髒缺血再灌註損傷(IRI)脩複過程中細胞週期蛋白E(cyclinE)和其依賴性激酶2(CDK2)錶達的變化,IMD可能的促進腎組織再生脩複的作用機製.方法 健康雄性Wistar大鼠,體重180~220g,共144隻隨機分為對照組、IRI組、轉空質粒組、轉IMD組.對照組和IRI組切除右腎;轉空質粒組、轉IMD組大鼠切除右腎後,在六氟化硫微泡(聲諾維)介導下將空質粒及IMD質粒轉染入左腎;1週後分彆製作腎髒IRI模型.每組于再灌註1d、2d、3d、4d、7d、14d時各取6隻留取腎組織標本.檢測各組腎組織中cyclinE與CDK2的錶達.結果 IRI組cyclin E、CDK2于再灌註後1d、2d、3d、4d、7d錶達逐漸增高,7d時到達最高峰,此後錶達逐漸降低,14d時降至最低,但仍有少量錶達,與對照組比較差異具有統計學意義(p<0.05).轉IMD組各項指標在第1d即開始顯著增高,第2d、3d、4d、7d呈進行性下降,至14d時恢複正常,與IRI組相比其差異具有統計學意義(p<0.05);轉空質粒組與IRI組以上指標差異無統計學意義.結論 IMD預處理大鼠腎髒缺血再灌註損傷後早期,cyclinE、CDK2的錶達明顯上調,提示IMD可能通過促進細胞週期進展從而加快腎組織再生脩複.
목적 관찰Intermedin(IMD)예처리대서신장결혈재관주손상(IRI)수복과정중세포주기단백E(cyclinE)화기의뢰성격매2(CDK2)표체적변화,IMD가능적촉진신조직재생수복적작용궤제.방법 건강웅성Wistar대서,체중180~220g,공144지수궤분위대조조、IRI조、전공질립조、전IMD조.대조조화IRI조절제우신;전공질립조、전IMD조대서절제우신후,재륙불화류미포(성낙유)개도하장공질립급IMD질립전염입좌신;1주후분별제작신장IRI모형.매조우재관주1d、2d、3d、4d、7d、14d시각취6지류취신조직표본.검측각조신조직중cyclinE여CDK2적표체.결과 IRI조cyclin E、CDK2우재관주후1d、2d、3d、4d、7d표체축점증고,7d시도체최고봉,차후표체축점강저,14d시강지최저,단잉유소량표체,여대조조비교차이구유통계학의의(p<0.05).전IMD조각항지표재제1d즉개시현저증고,제2d、3d、4d、7d정진행성하강,지14d시회복정상,여IRI조상비기차이구유통계학의의(p<0.05);전공질립조여IRI조이상지표차이무통계학의의.결론 IMD예처리대서신장결혈재관주손상후조기,cyclinE、CDK2적표체명현상조,제시IMD가능통과촉진세포주기진전종이가쾌신조직재생수복.
Objectives Intermedin(IMD)pretreatment in rat renal ischemia-reperfusion injury(IRI)during the repair process cyclin E(cyclinE)and its dependent kinase 2(CDK2)expression changes,IMD may promote kidney tissue regeneration and repair mechanisms.Methods Male Wistar rats weighing 180~220g,144were randomly divided into control group,IRI group,empty vector transfected group,turn IMD group.Control group and the removal of the right kidney IRI group; turn empty plasmid group,turn right kidney removed after the IMDgroup,the sulfur hexafluoride microbubbles(SonoVue)mediated plasmid and empty plasmid transfected into the left renal IMD ; were made after 1 week of renal IRI model.Each group in the reperfusion 1d,2d,3d,4d,7d,14dfrom each of six specimens from the time of renal tissues.Renal tissue were detected by cyclinE and CDK2 expression.Results IRI group cyclin E,CDK2 after reperfusion 1 d,2d,3d,4d,7d expression gradually increased,7d reach the peak time,then gradually decreased expression,14d when the minimum,but there is still a small amount of expression,compared with the control group the difference was significant(p < 0.05).IMD Group switch indicators began in 1d significantly increased on 2d,3d,4d,7d decreased progressively,from 14d to resume normal,compared with the IRI and the differences were statistically significant(p < 0.05); empty vector transfected group and the IRI group no significant difference between the above indicators.Conclusions IMD pretreatment in rat kidney after ischemia and reperfusion injury early,cyclinE,CDK2 expression was significantly increased,suggesting that IMD could promote cell cycle progression through to speed up the regeneration of kidney tissue.