当归预处理对脑缺血后VEGF和cyclin D1表达的影响

The Effect of Danggui Precondition on VEGF and Cyclin D1 Expression after Global Cerebral Ischemia

目的 研究全脑缺血后血管内皮生长因子 (vascularendothelialgrowthfactor ,VEGF)和细胞周期蛋白(cyclinD1)表达及当归注射液预处理的影响。 方法 6 6只健康沙土鼠 ,分为预处理组、对照组和正常组 ,预处理组经腹腔给予当归注射液后行双侧颈总动脉夹闭 10min制作全脑缺血再灌注模型 ,对照组经腹腔给予生理盐水后制作全脑缺血再灌注模型 ,正常组不作任何处理。于术后 2h、4h、8h、1d、2d 5个时间点采用免疫组织化学方法检测VEGF和cyclinD1表达的变化。 结果 全脑缺血再灌注 2h至 2d ,动物脑组织各区未见明显形态学改变。缺血后 2hVEGF表达开始增加 ,2d内持续上升 ;预处理组皮质下VEGF阳性神经元数目在再灌注 2h、4h、1d 3个时间点高于对照组 ,脉络组织VEGF平均光密度在再灌注 4h、8h、1d 3个时间点高于对照组 ,在再灌注 2d低于对照组。皮质III、IV层cyclinD1阳性神经元在再灌注 1d开始增加 ,在再灌注 1、2d 2个时间点预处理组低于对照组 (P <0 .0 5 )。结论 全脑缺血后VEGF和cyclinD1表达增强 ,当归注射液可促进VEGF高表达 ,同时又可抑制脉络组织的过度表达 ,并抑制cyclinD1的表达。

Objective To study the effect of danggui injection precondition on VEGF(vascular endotheliar growth factor) and cyclin D1 expression after global cerebral ischemia. Methods 66 gerbils were divided into three groups, 30 in precondition group which were administered with danggui injection intraperitonealy before bileteral common artery obligated for 10 minutes to develop global cerebral ischemia model, 30 in control group which received normal saline before cerebral ischemia operation, and still 6 in normal group without any treatment. At 2 h, 4 h, 8 h, 1 d, 2 d after operation, immunohistochemistry was used to evaluate the expressions of VEGF and cyclin D1 in brain tissue. Results No evident morphologic changes were detected after operation. VEGF expression began to increase at 2 h and kept increasing within 2 d. VEGF positive neurons in subcortex in precondition group were more than those in control group at 2 h, 4h and 1d. VEGF optical density in choroid tissue was higher than control group at 4 h, 8 h and 1 d, and lower at 2 d. Cyclin D1 positive neurons in III and IV layer of cortex began to increase at 8 h and were more than control group at 8 h, 1 d, 2 d (P<0.05). Conclusion After global cerebral ischemia, the expressions of VEGF and cyclin D1 were upregulated. Danggui injection precondition can promote the expression of VEGF to some degree and inhibit its overexpression in choroid tissue and inhibit the expression of cyclin D1.