Mechanism research of effect of platelet-rich plasma on flap neovascularization in diabetic rats by regulating SDF-1/CXCR4 signaling pathway
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摘要: 目的 观察富血小板血浆(PRP)对糖尿病大鼠背部皮瓣新生血管的影响,并分析血管内皮生长因子(VEGF)、基质细胞衍生因子(SDF-1)及趋化生长因子受体(CXCR4)的变化。 方法 将100只SD大鼠随机分为5组,各组20只;储备组制备PRP与贫血小板血浆(PPP),对照组正常饲养,其他组制备糖尿病病理模型;模型制备成功后,构建背部皮瓣,PRP组和PPP组分别以PRP和PPP进行局部干预。1周后观察新生血管,以ELISA试剂盒测定静脉血和局部组织VEGF水平,以免疫组化实验测定局部组织SDF-1与CXCR4表达。 结果 与对照组相比,模型组和PPP组的皮瓣存活率降低,新生血管数和VEGF含量减少,SDF-1和CXCR4表达水平降低;PRP组的VEGF含量减少,SDF-1和CXCR4表达水平升高;各项差异均有统计学意义(P<0.05)。与模型组和PPP组相比,PRP组的皮瓣存活率升高,新生血管数和VEGF含量增多,SDF-1和CXCR4表达水平升高;各项差异均有统计学意义(P<0.05)。 结论 PRP可提高糖尿病大鼠局部和全身VEGF水平,上调SDF-1与CXCR4表达,促进血管生成,可能为其促进糖尿病皮瓣愈合的重要机制之一。Abstract: Objective To observe the influence of platelet-rich plasma (PRP) on the back flap neovascularization in diabetic rats and analyze the changes of the levels of vascular endothelial growth factor(VEGF),stromal cell-derived factor(SDF-1) and chemokine growth factor receptor(CXCR4). Methods Total 100 SD rats were randomly divided into five groups with 20 in each group.The reserve group was prepared PRP and platelet poor plasma(PPP),the control group was normal feed,and the other three groups were made diabetic pathological model.After model success the back flaps were prepared.PRP and PPP group were treated by PRP and PPP intervene locally.After 1 week,the angiogenesis was observed,VEGF level was measured by ELISA and SDF-1 and CXCR4 were detected by immunohistochemistry assay. Results When compared to control group,the flap survival rates of model group and PPP group were reduced,new blood vessel number and VEGF level were reduced,and SDF-1 and CXCR4 expression were reduced.The differences were statistically significant(P<0.05).Compared to model group and PPP group,flap survival rate of PRP Group was higher,the new blood vessel number and VEGF level were higher,and SDF-1 and CXCR4 expression were higher.The differences were statistically significant(P<0.05). Conclusion PRP can improve the local and systemic VEGF level of diabetic rats,increase the expression of SDF-1 and CXCR4,and promote angiogenesis,which might be the mechanisms for promoting the healing skin flap.
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