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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。
OBJECTIVE: To observe the expression of MAP-2 and NTP in the brain tissue of cats treated with basic fibroblast growth factor (bFGF) for different periods of ischemia-reperfusion, and to investigate the effect of bFGF on ischemia-reperfusion Possible mechanism of brain injury. Methods: Thirty healthy domestic cats were randomly divided into normal saline control group and bFGF treatment group. The left middle orbital approach was used to create a model of middle cerebral artery ischemia reperfusion. Neurological deficit scores were assessed by Philip’s neurological deficit scores of cats at preoperative, 24, 48, and 7 days after reperfusion. The levels of MAP-2 and MAP-2 at different time points after ischemia-reperfusion were detected by immunohistochemistry SP method. NTP protein expression, immunopositive cell count. Results: After 48h of ischemia-reperfusion, the damage of neurological function in the treatment group was significantly reduced compared with the control group, and the number of MAP-2 and NTP-positive cells was also significantly increased compared with the control group. CONCLUSION: bFGF can reduce the neuronal damage and promote the growth of nerve fibers in the brain tissue after ischemia-reperfusion by inducing the expression of MAP-2 and NTP protein, so as to improve the impaired neurological function.