摘要
目的探讨促肝细胞生长因子(pHGF)对脑缺血再灌注损伤神经元的抗凋亡作用及机制。方法36只健康雄性W istar大鼠,随机分为缺血对照组和pHGF治疗组,再随机分为再灌注6h、12h、24h组3个亚组。采用动脉线栓法建立大鼠脑缺血再灌注模型,于各观察时间点处死大鼠取脑组织制切片,应用TUNEL法和免疫组化法检测神经元凋亡及bc l-2、p53蛋白表达情况。结果各观察时间点,pHGF治疗组凋亡细胞数及p53蛋白阳性细胞数较缺血对照组明显减少(P<0.05),pHGF治疗组bc l-2蛋白阳性细胞数较缺血对照组明显增多(P<0.01)。结论pHGF具有抑制脑缺血再灌注损伤神经元凋亡的作用,其作用机制与调节bc l-2、p53蛋白表达有关。
Objective To explore the anti-apoptosis effect and mechanism of pHGFon cerebral isehemia-reperfusion injuried neurons. Methods 36 healthy male Wistar rats were divided into ischemie control group and pHGF treatment groups at random, then randomly divided into reperfusion 6h, 12h and 24h three sub-groups. The model of cerebral isehemia-reperfusion injury was established in rats by artery thread law, rats were killed at different time points and brain regions were used respectively to detect neuronal apoptosis and bcl-2, p53 protein expression was detected by TUNEL and immunohistoehemical method. Results At each observation time point, apoptosis cells and p53 protein positive cells in the pHGF treatment group were significantly less than the ischemie control group ( P 〈 0.05 ), and bcl-2 positive cells in the pHGF treatment group were significantly more than the ischemie control group( P 〈 0. 01 ). Conclusion pHGF can inhibit cerebral ischemia-reperfusion injuried neuronal apoptosis, and regulation of bcl-2 and p53 protein expression is the probable anti-apoptosis mechanism.
出处
《中风与神经疾病杂志》
CAS
CSCD
北大核心
2009年第1期11-13,共3页
Journal of Apoplexy and Nervous Diseases