温州医科大学学报
溫州醫科大學學報
온주의과대학학보
Journal of Wenzhou Medical University
2015年
2期
115-118
,共4页
李金海%陈辉春%戴华卫%张海峰%王烈
李金海%陳輝春%戴華衛%張海峰%王烈
리금해%진휘춘%대화위%장해봉%왕렬
脂多糖%内皮,血管%细胞增殖%细胞凋亡
脂多糖%內皮,血管%細胞增殖%細胞凋亡
지다당%내피,혈관%세포증식%세포조망
lipopolysaccharide%endothelium,vascular%proliferation%apoptosis
目的:观察脂多糖(LPS)对体外培养的人脐血内皮祖细胞(EPCs)增殖及凋亡的影响。方法:以密度梯度离心法获取人脐血EPCs,体外诱导分化并鉴定。实验分对照组及不同浓度(2.5、5.0、10.0、20.0 mmol/L)LPS组。四氮唑蓝(MTT)法检测细胞增殖能力,流式细胞仪测凋亡率及细胞周期。结果:①10.0 mmol/L组促进EPCs增殖,20.0 mmol/L组抑制EPCs增殖,差异有统计学意义(P<0.05),其余2组对EPCs增殖能力无显著影响,与对照组比差异无统计学意义(P>0.05)。②20.0 mmol/L组促进EPCs凋亡,差异有统计学意义(P<0.05)。其余各组对EPCs凋亡率无明显影响,与对照组比较差异均无统计学意义(P>0.05)。③10.0、20.0 mmol/L组影响细胞周期,10.0 mmol/L组G0/G1期细胞减少,S和G2/M期增加;20.0 mmol/L组发生S期阻滞,G2/M期细胞减少,与对照组比差异有统计学意义(P<0.05)。结论:LPS对EPCs增殖能力及凋亡的影响与其浓度有关,当浓度为20.0 mmol/L时抑制增殖并促进凋亡。
目的:觀察脂多糖(LPS)對體外培養的人臍血內皮祖細胞(EPCs)增殖及凋亡的影響。方法:以密度梯度離心法穫取人臍血EPCs,體外誘導分化併鑒定。實驗分對照組及不同濃度(2.5、5.0、10.0、20.0 mmol/L)LPS組。四氮唑藍(MTT)法檢測細胞增殖能力,流式細胞儀測凋亡率及細胞週期。結果:①10.0 mmol/L組促進EPCs增殖,20.0 mmol/L組抑製EPCs增殖,差異有統計學意義(P<0.05),其餘2組對EPCs增殖能力無顯著影響,與對照組比差異無統計學意義(P>0.05)。②20.0 mmol/L組促進EPCs凋亡,差異有統計學意義(P<0.05)。其餘各組對EPCs凋亡率無明顯影響,與對照組比較差異均無統計學意義(P>0.05)。③10.0、20.0 mmol/L組影響細胞週期,10.0 mmol/L組G0/G1期細胞減少,S和G2/M期增加;20.0 mmol/L組髮生S期阻滯,G2/M期細胞減少,與對照組比差異有統計學意義(P<0.05)。結論:LPS對EPCs增殖能力及凋亡的影響與其濃度有關,噹濃度為20.0 mmol/L時抑製增殖併促進凋亡。
목적:관찰지다당(LPS)대체외배양적인제혈내피조세포(EPCs)증식급조망적영향。방법:이밀도제도리심법획취인제혈EPCs,체외유도분화병감정。실험분대조조급불동농도(2.5、5.0、10.0、20.0 mmol/L)LPS조。사담서람(MTT)법검측세포증식능력,류식세포의측조망솔급세포주기。결과:①10.0 mmol/L조촉진EPCs증식,20.0 mmol/L조억제EPCs증식,차이유통계학의의(P<0.05),기여2조대EPCs증식능력무현저영향,여대조조비차이무통계학의의(P>0.05)。②20.0 mmol/L조촉진EPCs조망,차이유통계학의의(P<0.05)。기여각조대EPCs조망솔무명현영향,여대조조비교차이균무통계학의의(P>0.05)。③10.0、20.0 mmol/L조영향세포주기,10.0 mmol/L조G0/G1기세포감소,S화G2/M기증가;20.0 mmol/L조발생S기조체,G2/M기세포감소,여대조조비차이유통계학의의(P<0.05)。결론:LPS대EPCs증식능력급조망적영향여기농도유관,당농도위20.0 mmol/L시억제증식병촉진조망。
Objective:To investigate the effect of proliferation, apoptosis and cell cycle of lipopolysac-charide (LPS) on human umbilical vein endothelial progenitor cells. Methods:mononuclear cells were isolated from human umbilical cord blood. Mononuclearcells (MNCs) were isolated from human umbilical cord blood in vitro by Ficoll density gradient centrifugation. EPCs were characterized as adherent cells with double positive to DiI-acLDL uptake and lectin binding by direct lfuorescent staining under a laser scanning confocal microscope. There were ifve groups. The control group and four LPS concentration groups:2.5, 5.0, 10.0, 20.0 mmol/L. MTT was used to detect cell apoptosis and cell cycle. Results:①10.0 mmol/L LPS promotes proliferation of EPCs, while 20.0 mmol/L LPS inhibits the proliferation of endothelial progenitor cells (P<0.05).②20.0 mmol/L LPS promotes apoptosis of EPCs, compared with the control, the difference was signiifcant (P<0.05).③LPS at the concentration of 10.0 mmol/L reduces cells at G0/G1 phase and increases S and G2/M phase cells;20.0 mmol/L LPS induces EPCs blockade at S phase, G2/M phase cells decreased, compared with the control, the difference was signiifcant (P<0.05). Conclusion:10.0 mmol/L LPS promotes the proliferation of EPCs. 20.0 mmol/L LPS inhibits the proliferation and promotes apoptosis of EPCs.