中华肾脏病杂志
中華腎髒病雜誌
중화신장병잡지
2013年
3期
199-203
,共5页
刘昊%吴然%贾瑞鹏%仲冰%于澎%赵炎
劉昊%吳然%賈瑞鵬%仲冰%于澎%趙炎
류호%오연%가서붕%중빙%우팽%조염
动力学%微环境%祖细胞%缺血预适应
動力學%微環境%祖細胞%缺血預適應
동역학%미배경%조세포%결혈예괄응
Dynamics%Microenvironment%Progenitor cell%Ischemic preconditioning
目的 探讨缺血预适应(IPC)对肾脏缺血再灌注损伤(IR)后内源性内皮祖细胞(EPC)归巢动力学的影响及意义.方法 60只雄性SD大鼠切除右肾1周后被随机分为3组:(1)对照组:仅游离左肾动脉;(2)缺血再灌注损伤组(IR组):夹闭左肾动脉40 min后恢复灌注;(3)缺血预适应组(IPC组):夹闭肾蒂前给予15 min缺血、10 min再灌注预处理,余同IR组.术后3、12、24、72 h留取大鼠静脉血、肾、脾、肺脏.血生化检测及组织病理学检查评估各组大鼠术后肾损伤程度;流式细胞术观察IPC对EPC归巢动力学影响.结果 IPC组血肌酐、尿素氮及肾小管损伤评分均低于同时间点IR组.与对照组或IR组相比,IPC组大鼠外周血EPC数量在术后12、24 h升高(P<0.05);与同时间点IR组比较,IPC组肾组织EPC数量在12、24 h增高[(11.36±0.66)%比(6.37±0.69)%,(6.31±0.70)%比(4.40±0.60)%,均P<0.05];IPC组术后12h肺脏EPC数量高于IR组[(2.95±0.66)%比(1.78±0.59)%,P<0.05]及对照组[(2.95±0.66)%比(1.66±0.61)%,P< 0.05].IPC组术后72 h脾脏EPC数量高于同时间点IR组和对照组[(0.55±0.06)%比(0.34±0.07)%、(0.31±0.06)%,均P< 0.05].结论 IPC可动员内源性EPC随血流归巢至损伤肾脏.EPC尚可在肺脏、脾脏中聚集.
目的 探討缺血預適應(IPC)對腎髒缺血再灌註損傷(IR)後內源性內皮祖細胞(EPC)歸巢動力學的影響及意義.方法 60隻雄性SD大鼠切除右腎1週後被隨機分為3組:(1)對照組:僅遊離左腎動脈;(2)缺血再灌註損傷組(IR組):夾閉左腎動脈40 min後恢複灌註;(3)缺血預適應組(IPC組):夾閉腎蒂前給予15 min缺血、10 min再灌註預處理,餘同IR組.術後3、12、24、72 h留取大鼠靜脈血、腎、脾、肺髒.血生化檢測及組織病理學檢查評估各組大鼠術後腎損傷程度;流式細胞術觀察IPC對EPC歸巢動力學影響.結果 IPC組血肌酐、尿素氮及腎小管損傷評分均低于同時間點IR組.與對照組或IR組相比,IPC組大鼠外週血EPC數量在術後12、24 h升高(P<0.05);與同時間點IR組比較,IPC組腎組織EPC數量在12、24 h增高[(11.36±0.66)%比(6.37±0.69)%,(6.31±0.70)%比(4.40±0.60)%,均P<0.05];IPC組術後12h肺髒EPC數量高于IR組[(2.95±0.66)%比(1.78±0.59)%,P<0.05]及對照組[(2.95±0.66)%比(1.66±0.61)%,P< 0.05].IPC組術後72 h脾髒EPC數量高于同時間點IR組和對照組[(0.55±0.06)%比(0.34±0.07)%、(0.31±0.06)%,均P< 0.05].結論 IPC可動員內源性EPC隨血流歸巢至損傷腎髒.EPC尚可在肺髒、脾髒中聚集.
목적 탐토결혈예괄응(IPC)대신장결혈재관주손상(IR)후내원성내피조세포(EPC)귀소동역학적영향급의의.방법 60지웅성SD대서절제우신1주후피수궤분위3조:(1)대조조:부유리좌신동맥;(2)결혈재관주손상조(IR조):협폐좌신동맥40 min후회복관주;(3)결혈예괄응조(IPC조):협폐신체전급여15 min결혈、10 min재관주예처리,여동IR조.술후3、12、24、72 h류취대서정맥혈、신、비、폐장.혈생화검측급조직병이학검사평고각조대서술후신손상정도;류식세포술관찰IPC대EPC귀소동역학영향.결과 IPC조혈기항、뇨소담급신소관손상평분균저우동시간점IR조.여대조조혹IR조상비,IPC조대서외주혈EPC수량재술후12、24 h승고(P<0.05);여동시간점IR조비교,IPC조신조직EPC수량재12、24 h증고[(11.36±0.66)%비(6.37±0.69)%,(6.31±0.70)%비(4.40±0.60)%,균P<0.05];IPC조술후12h폐장EPC수량고우IR조[(2.95±0.66)%비(1.78±0.59)%,P<0.05]급대조조[(2.95±0.66)%비(1.66±0.61)%,P< 0.05].IPC조술후72 h비장EPC수량고우동시간점IR조화대조조[(0.55±0.06)%비(0.34±0.07)%、(0.31±0.06)%,균P< 0.05].결론 IPC가동원내원성EPC수혈류귀소지손상신장.EPC상가재폐장、비장중취집.
Objectives To investigate the impact of ischemic preconditioning (IPC) on dynamics of homing of endothelial progenitor cells (EPCs) after renal ischemia reperfusion injury (IR).Methods Sixty male Sprague-Dawley rats were randomly divided into three groups after right-side kidney nephrectomy:for sham-operated rats,lumbotomy without vascular clamping was performed; IR rats were clamped renal blood vessels for 40 minutes while IPC rats were pre-treated with 15 min ischemia and 10 min reperfusion.At 3,12,24 h,and 3 days after reperfusion,the pool of circulating,kidneys,lungs and spleens were harvested.The extent of renal injury was assessed by biochemical and histological examination.The dynamics of homing of EPCs was observed by flow cytometry.Results The rats in IPC group exhibited significant improvements in renal function and morphology.Compared with IR group and sham group,the number of EPCs in blood was increased in the IPC group at 12 h and 24 h after reperfusion (P < 0.05).The number of EPCs in kidney was increased at all times point in the IPC group and IR group as compared to the sham group (P < 0.05.In addition,EPCs number was increased in IPC group compared with the IR group at 12 h and 24 h [(11.36±0.66)% vs (6.37±0.69)%,(6.31±0.70)% vs (4.40±0.60)%,all P< 0.05].Compared with IR group and sham group,the number of EPCs in the lung was increased in the IPC groups at 12 h after reperfusion [(2.95±0.66)% vs (1.78±0.59)%,(1.66±0.61)%,all P < 0.05].The number of EPCs in spleen was increased in the IPC group at 72 h as compared with the IR group and sham group [(0.55±0.06)% vs (0.34±0.07)%,(0.31±0.06)%,all P < 0.05].Conclusions Endogenous EPCs may home to injured kidney after IPC.EPCs can also gather in the lungs and spleen.