内皮祖细胞在早期急性肾缺血再灌注损伤中的抗凋亡作用观察-东南大学学报医学版

内皮祖细胞在早期急性肾缺血再灌注损伤中的抗凋亡作用观察

单位：1. 东南大学医学院,江苏南京 210009;
2. 南京医科大学附属南京第一医院泌尿外科,江苏南京 210006

分类号：R691.5

出版年·卷·期（页码）：2012·31·第五期（581-585）

摘要：

目的:观察内皮祖细胞(EPC)移植对急性肾缺血再灌注损伤(IRI)早期的治疗作用及其对肾小管上皮细胞凋亡的影响,探讨其可能的肾脏保护机制。方法:大鼠骨髓单个核细胞体外定向诱导、扩增获取EPC并标记。SD大鼠随机分为3组:移植组进行急性肾缺血再灌注操作后行EPC移植;IRI组缺血再灌注后注入等量生理盐水;假手术组假手术后注入EPC。检测IRI后24、48 h 3组大鼠的肾功能,观察IRI后72 h 3组大鼠肾组织损伤、肾小管上皮细胞凋亡、EPC在肾组织中的归巢情况。结果:肾IRI后72 h,移植组肾脏皮髓交界处内可见少量CM-Dil阳性细胞。移植组大鼠较对照组肾功能明显改善(P<0.05),肾损伤明显减轻(P<0.01),肾小管上皮细胞凋亡明显减少(P<0.01),血管内皮生长因子(VEGF)表达水平显著升高(P<0.05)。结论:骨髓源性EPC移植对急性肾IRI有治疗作用,其可能机制是通过减少肾小管上皮细胞凋亡来减轻IRI早期的肾损害。

Objective: To evaluate the therapeutic effects of endothelial progenitor cells(EPC) transplantation in the early phase of acute renal ischemia reperfusion injury(IRI)in rats and their impact on tubular epithelial cell apoptosis. Methods: Bone marrow-derived monocytes cells of rats were isolated and induced differentiation into EPC in vitro. SD rats were randomly divided into three groups. Rats of transplanted group were induced acute renal IRI, then transplanted EPC immediately after reperfusion. IRI group were induced renal IRI and then infused with saline instead. Sham group were infused with EPC after shame operation. Renal function of three groups was detected at 24 and 48 h after IRI. Kidney morphology, apoptosis and the homing of EPC in IRI kidney were observed 72 h after IRI. Results: 72 hours after transplantation, EPC derived CM-Dil positive cell were detected at the junction of the cortex and medulla of the renal tissues of transplanted rats. Compared with IRI group, the renal functional and structural damage were significantly ameliorated (P<0.05), tubular epithelial cell apoptosis was reduced significantly in transplanted group (P<0.01). And the expression levels of vascular endothelial growth factor (VEGF) were also increased greatly in transplanted group (P<0.05). Conclusion: Bone marrow-derived EPC transplantation is curative for acute renal IRI in rats. EPC might ameliorate renal morphology and function after renal IRI by reducing tubular epithelial cell apoptosis.

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