碱性成纤维细胞生长因子治疗猫急性脑梗死的作用机制研究

目的:观察碱性成纤维生长因子(bFGF)处理的缺血再灌注不同时程的猫脑组织中微管相关蛋白(MAP-2)和神经丝蛋白(NTP)的表达,探讨bFGF治疗缺血性脑损伤的可能作用机制。方法:健康家猫30只,随机分为生理盐水对照组和bFGF治疗组。采用左侧眼眶入路制作大脑中动脉缺血再灌注模型。于术前和再灌注24h、48h和7d,采用Philip的猫脑缺血神经功能评分标准进行神经功能缺损评分;应用免疫组织化学SP法检测缺血再灌注不同时程的脑组织MAP-2及NTP蛋白表达,进行免疫阳性细胞计数。结果:缺血再灌注48h后,治疗组动物神经功能受损程度较对照组明显减轻,MAP-2及NTP蛋白阳性细胞数目较对照组也显著增加。结论:bFGF通过诱导MAP-2及NTP蛋白的表达,减轻了缺血再灌注脑组织的神经元损伤和促进了神经纤维生长,从而改善受损的神经功能。

Mechanism of bFGF Action for Treating Acute Cerebral Infarction in Cats

Aim:To observe the expressions of microtubule associated protein 2(MAP-2) and neural thread protein(NTP) in brains of acute cerebral infarction cats treated by using basic fibroblast growth factor(bFGF) ,and to explore a possible mechanism of bFGF action for treating ischemic cerebral injury. Methods:30 healthy adult cats were randomly and equally divided into the control group and bFGF-treated group. All animals were operated to establish the feline models of cerebral focal ischemia-reperfusion by the approach of left transorbital. The score of neurological defects was evaluated by Philip's criteria score,and the expressions of MAP-2 and NTP were observed by immunohistochemisty before operation and after ischemia for 2 h and reperfusion for 24 h,48 h and 7 d. The number of the positive cells was calculated under the microscope. Results:After ischemia/reperfusion for 48 h,the score of neurological defects was obviously decreased,but both of MAP-2 and NTP positive cellular numbers were distinctly increased in the cat's brains of bFGF-treated group compared with the animals of control group. Conclusion:bFGF had a remarkable therapeutic effect to acute cerebral infarction by inducing MAP-2 and NTP expressions,which can relieve the neuronal injury caused by ischemia/reperfusion,accelerate the growth of nerve fibers and improve the nervous function.