PEDF、END 在UUO 肾组织的表达及ADSCs 对其的影响

Expressions of PEDF and endostatin in rat kidney after unilateral ureteral obstruction and effect of adipose-derived stem cells on them

摘要:

目的 动态观察大鼠单侧输尿管梗阻（UUO）肾组织中色素上皮衍生因子（PEDF）及内皮抑素（END）的变化，以及脂肪干细胞（ADSCs）对其的影响。方法 复制UUO 动物模型，以ADSCs 进行干预，选取UUO 术后第3、7 和14 天为时间点，观察大鼠在UUO 后肾损伤及纤维化的进程，以及PEDF 和END蛋白的表达变化。结果 肾损伤、纤维化程度及PEDF 的表达随梗阻时间延长而加重或增加。END 在术后先增加后降低，但仍高于对照组。ADSCs 干预在各个时间点均能使END 和PEDF 的表达降低。结论 UUO后PEDF 和END 蛋白表达上调可能是梗阻后微血管损伤、血管生成调节异常介导的微血管闭塞产生的重要机制之一。ADSCs 干预可通过抑制PEDF 和END 的表达，促进损伤血管的修复和新生血管的生成。

Abstract:

Objective To observe the dynamic changes of pigment epithelium-derived factor (PEDF) and endostatin (END) expressions in renal tissues 3, 7 and 14 days after unilateral ureteral obstruction (UUO) in rats and the expression changes after the intervention of adipose-derived stem cells, so as to explore the possible mechanism of PEDF and END in UUO and the relationship between them and the effect of adipose-derived stem cells on the expressions of PEDF and END in the course of UUO. Methods Seventy healthy adult male SD rats were randomly divided into sham operation control group (10 rats), UUO group (30 rats) and intervention group (30 rats). The UUO model was produced by unilateral ureteral obstruction and the rats in the intervention group were injected with adipose-derived stem cells in 24 hours. On the 3rd, 7th and 14th day after ureteral obstruction, the progression of renal injury and fibrosis and the expressions of PEDF and END in rats were observed. Results The renal injury and fibrosis got more severe with the prolongation of the time of obstruction, the expressions of PEDF and END in the UUO group were higher than those of the control group at each time point. The expressions of END and PEDF were decreased at all time points after intervention by adipose-derived stem cells. Conclusions The upregulation of PEDF and END after UUO may be one of the important mechanisms of microvascular occlusion mediated by regulation abnormality of microvascular injury and angiogenesis. Intervention of adipose-derived stem cells can promote the repair of vascular injury and angiogenesis by inhibiting the expressions of PEDF and END.