血管内皮生长因子对神经细胞的保护作用及机制

目的 探讨VEGF对体外培养的神经元保护作用及机制。方法 体外培养大鼠皮质神经元细胞，建立神经细胞缺氧缺糖/再灌注损伤模型(OGSD)，在加入VEGF基础上，加入VEGFR-2/Flk-1受体抑制剂SU1498；检测以下指标：①观察细胞形态学变化②细胞活力：MTT法③线粒体跨膜电位④凋亡相关蛋白：Bc1-2和Bax表达。结果 ①OGSD组、VEGF164+SU1498组细胞损害重，VEGF组细胞损害轻(p<0.05)；②OGSD组、VEGF164+SU1498组细胞活力下降明显(p<0.05)，而VEGF组与正常组无明显区别；③OGSD组、VEGF164+SU1498组线粒体跨膜电位不稳定(p<0.05)，VEGF能稳定线粒体跨膜电位；④OGSD组、VEGF164+SU1498组Bcl- 2、Bax蛋白表达均增多，VEGF组Bcl- 2蛋白表达增多最明显(p<0.01)，而Bax蛋白表达增多最不明显(p<0.01)。结论 VEGF对神经元起直接的保护作用，并通过与VEGFR-2受体结合减少了缺血、缺氧下培养的体外神经元细胞的凋亡。

Neuroprotective effects and mechanisms of Vascular endothelial growth factor

ObjectiveTo observe neuroprotective effects and mechanisms of Vascular endothelial growth factor on vitro neurocyte.Methods Culturing neural cell line of cerebral cortex of rat in oxygen—glucose—serum deprivation(OGSD),then were randomly divided into four groups, normal group,OGSD group,VEGF group and VEGF164 added SU1498 group;detecting cell morphological change ,cell vigor through MTT, mitochondrial transmembrane potential and expression of Bcl-2／Bax.Results Impairment of VEGF group is less than OGSD group and VEGF164 added SU1498 group(p<0.05); VEGF group could maintain mitochondrial transmembrane potential,but OGSD group and VEGF164 added SU1498 group were opposite(p<0.05); Compared with OGSD group and VEGF164 added SU1498 group， Bcl-2 expression in VEGF group showed an obvious increase(p<0.01)， while Bax expression in VEGF group was opposite (p<0.01).Conclusions VEGF had direct neuroprotective effects on neurons, which may be mediated in vitro through VEGFR2/Flk-1 receptors,and decreased apoptosis on vitro neurocyte.