论文部分内容阅读
[目的]探讨VEGF/ERK信号转导通路在蛛网膜下腔出血(SAH)后早期脑损伤中的分子机制。[方法]采用非开颅血管内穿线法制备大鼠SAH模型,将动物随机分为control组、sham组及SAH组。术后24h取材行颅底解剖学检查,HE染色观察大脑中动脉(MCA)形态学改变,原位杂交法检测MCAVEGF mRNA的表达,免疫蛋白印记法检测大脑动脉VEGF,p-ERK1/2蛋白表达,TUNEL法检测MCA内皮细胞凋亡。[结果]SAH24hMCA出现严重的血管痉挛;VEGF mRNA阳性信号明显增强,VEGF、p-ERK1/2蛋白显著升高(P﹤0.05,ANOVA),MCA内皮细胞TUNEL显色阳性。SAH24hVEGF与p-ERK1/2蛋白表达呈正相关(r=0.722,P﹤0.01)。[结论]VEGF通过激活ERK途径,促进SAH后脑动脉内皮细胞凋亡,参与SAH后早期脑损伤的病理进程。
[Objective] To explore the molecular mechanism of VEGF / ERK signal transduction pathway in early brain injury after subarachnoid hemorrhage (SAH). [Methods] SAH model was prepared by intranasal non-craniotomy. The animals were randomly divided into control group, sham group and SAH group. The skull base anatomy was performed 24 h after operation. Morphological changes of middle cerebral artery (MCA) were observed by HE staining. The expression of MCAVEGF mRNA was detected by in situ hybridization. The expressions of VEGF and p-ERK1 / 2 were detected by immunohistochemistry TUNEL method was used to detect the apoptosis of MCA endothelial cells. [Results] Severe vasospasm occurred in SAH24hMCA, the positive signal of VEGF mRNA was significantly increased, the protein of VEGF and p-ERK1 / 2 were significantly increased (P <0.05, ANOVA), and the positive staining of TUNEL in MCA endothelial cells. There was a positive correlation between SAH24hVEGF and p-ERK1 / 2 protein expression (r = 0.722, P <0.01). [Conclusion] VEGF can promote the apoptosis of cerebral arterial endothelial cells after SAH by activating the ERK pathway and participate in the pathological process of early brain injury after SAH.