中华风湿病学杂志
中華風濕病學雜誌
중화풍습병학잡지
CHINESE JOURNAL OF RHEUMATOLOGY
2011年
8期
541-545
,共5页
褚宇东%李荣山%乔晞%孙秀丽
褚宇東%李榮山%喬晞%孫秀麗
저우동%리영산%교희%손수려
再灌注损伤%细胞周期蛋白类%细胞周期蛋白质依赖激酶类%再生%肾脏%Intermedin
再灌註損傷%細胞週期蛋白類%細胞週期蛋白質依賴激酶類%再生%腎髒%Intermedin
재관주손상%세포주기단백류%세포주기단백질의뢰격매류%재생%신장%Intermedin
Reperfusion injury%Cyclins%Cyclin-dependent kinase%Regeneration%Kidney%Intermedin
目的 观察Intermedin(IMD)预处理对大鼠肾脏缺血再灌注损伤(IRI)修复过程中细胞周期蛋白(cyclin)D1、cyclin E以及其依赖性激酶(CDKs)表达的影响,从而探讨IMD在这一过程中促进肾组织再生修复的作用机制.方法 健康雄性Wistar大鼠共144只,体质量180～220 g,随机分为对照组、IRI组、转空质粒组、转IMD组,每组36只.IRI组切除右肾后钝性分离左侧腹主动脉及肾动脉;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.每组于再灌注第1、2、3、4、7、14天时各取6只留取肾组织标本.检测各组肾组织中cyclin D1与CDK4,cyclinE与CDK2的表达.统计学处理采用单因素方差分析和t检验.结果 IRI组cyclin D1、cyclin E以及CDK4、CDK2于再灌注后第1、2、3、4、7天表达逐渐增高,第7天时到达最高峰,第14天时仍有少量表达,与对照组比较差异有统计学意义(F值=54.92,69.69,61.28,77.38,P均＜0.05).转IMD组上述指标在第1天即开始显著增高,第2、3、4、7天呈进行性下降,至第14天时恢复正常,与IRI组相比差异具有统计学意义(F值=54.92,69.60,61.28,77.38,P均＜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预处理在大鼠肾脏缺血再灌注损伤后早期能使cyclinD1、cyclinE以及CDK4、CDK2的表达明显上调,这一机制可能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)預處理對大鼠腎髒缺血再灌註損傷(IRI)脩複過程中細胞週期蛋白(cyclin)D1、cyclin E以及其依賴性激酶(CDKs)錶達的影響,從而探討IMD在這一過程中促進腎組織再生脩複的作用機製.方法 健康雄性Wistar大鼠共144隻,體質量180～220 g,隨機分為對照組、IRI組、轉空質粒組、轉IMD組,每組36隻.IRI組切除右腎後鈍性分離左側腹主動脈及腎動脈;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.每組于再灌註第1、2、3、4、7、14天時各取6隻留取腎組織標本.檢測各組腎組織中cyclin D1與CDK4,cyclinE與CDK2的錶達.統計學處理採用單因素方差分析和t檢驗.結果 IRI組cyclin D1、cyclin E以及CDK4、CDK2于再灌註後第1、2、3、4、7天錶達逐漸增高,第7天時到達最高峰,第14天時仍有少量錶達,與對照組比較差異有統計學意義(F值=54.92,69.69,61.28,77.38,P均＜0.05).轉IMD組上述指標在第1天即開始顯著增高,第2、3、4、7天呈進行性下降,至第14天時恢複正常,與IRI組相比差異具有統計學意義(F值=54.92,69.60,61.28,77.38,P均＜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預處理在大鼠腎髒缺血再灌註損傷後早期能使cyclinD1、cyclinE以及CDK4、CDK2的錶達明顯上調,這一機製可能促進細胞週期進展從而加快腎組織再生脩複.
목적 관찰Intermedin(IMD)예처리대대서신장결혈재관주손상(IRI)수복과정중세포주기단백(cyclin)D1、cyclin E이급기의뢰성격매(CDKs)표체적영향,종이탐토IMD재저일과정중촉진신조직재생수복적작용궤제.방법 건강웅성Wistar대서공144지,체질량180～220 g,수궤분위대조조、IRI조、전공질립조、전IMD조,매조36지.IRI조절제우신후둔성분리좌측복주동맥급신동맥;전공질립조、전IMD조대서절제우신후,재륙불화류미포(성낙유)개도하장공질립급IMD질립전염입좌신;1주후분별제작신장IRI모형.매조우재관주제1、2、3、4、7、14천시각취6지류취신조직표본.검측각조신조직중cyclin D1여CDK4,cyclinE여CDK2적표체.통계학처리채용단인소방차분석화t검험.결과 IRI조cyclin D1、cyclin E이급CDK4、CDK2우재관주후제1、2、3、4、7천표체축점증고,제7천시도체최고봉,제14천시잉유소량표체,여대조조비교차이유통계학의의(F치=54.92,69.69,61.28,77.38,P균＜0.05).전IMD조상술지표재제1천즉개시현저증고,제2、3、4、7천정진행성하강,지제14천시회복정상,여IRI조상비차이구유통계학의의(F치=54.92,69.60,61.28,77.38,P균＜0.05);전공질립조여IRI조이상지표차이무통계학의의.결론 IMD예처리재대서신장결혈재관주손상후조기능사cyclinD1、cyclinE이급CDK4、CDK2적표체명현상조,저일궤제가능촉진세포주기진전종이가쾌신조직재생수복.
Objective To observe the effect of intermedin (IMD) preconditioning on cyclin D1, cyclin E and CDKs expression, and explore its role in.promoting kidney tissue regeneration after renal ischemiareperfusion injury. Methods One hundred and forty-four healthy male Wistar rats were randomly divided into four groups: sham operation (S) group, ischemia-reperfusion injury (IR) group, empty plasmid (EP) group and IMD group. In the IR group, after the right kidney was excised, the aorta abdominalis and left renal artery were bluntly dissected in EP and IMD group, empty plasmid and IMD plasmid were transfected into the left kidney using ultrasound-micro-bubble (SonoVue) mediated system, respectively. One week later, renal IRI model was made by clasping the left renal artery for 45 min. After 1, 2, 3, 4, 7 and 14 day of reperfusion, the kidney in each group was collected to detect the expression of cyclin D1, cyclin E, CDK4 and CDK2 by western blot analysis or enzyme-linked immunosorbent assay (ELISA). Results Compared with S group, the expression of cyclin D1, cyclin E, CDK4 and CDK2 was significantly up-regulated in day 1, 2,3, 4, 7 and 14 in IR group. And the above index increased gradually after reperfusion, and reached the peak at day 7 (F=54.92, 69.60, 61.28, 77.38, P＜0.05). While in IMD group, these indexes reached the peak at day 1, then progressively declined, and could not be detected at day 14 (compared with the IR group, F=54.92, 69.60, 61.28, 77.38, P＜0.05). Conclusion IMD preconditioning can up-regulate the expression of cyclin D1, cyclin E, CDK2 and CDK4 in the early phase of renal ischemia-reperfusion injury that may accelerate repair of renal tissue, at least by part, by enhancinge cell proliferation.
