碱性成纤维细胞生长因子对大鼠局灶性脑缺血再灌注后脑细胞内游离钙变化的影响

背景:碱性成纤维细胞生长因子可促进体外培养的神经元存活及突起生长,拮抗兴奋性氨基酸毒性,对中枢神经系统功能恢复起重要作用,能否通过影响脑细胞内游离钙离子浓度对缺血脑组织起保护作用.目的:从细胞水平探讨碱性成纤维细胞生长因子对大鼠局灶性脑缺血再灌注损伤时神经细胞内游离Ca2+浓度变化的影响.设计:完全随机对照实验.单位:郑州大学第二附属医院神经内科.材料:实验于2003-08/12在郑州大学第二附属医院神经内科实验室完成.24只SD大鼠随机分为假手术组、缺血再灌注组和碱性成纤维细胞生长因子治疗组,每组8只.方法:缺血再灌注组及碱性成纤维细胞生长因子治疗组采用线栓法建立大脑中动脉闭塞模型;假手术组除不插线外,余同其他两组.碱性成纤维细胞生长因子治疗组于缺血后即刻腹腔注射10μg/kg碱性成纤维细胞生长因子,其余两组腹腔注射等量生理盐水.各组大鼠于缺血再灌注24 h检测脑细胞游离钙浓度.主要观察指标:各组大鼠缺血再灌注24 h脑细胞游离钙浓度.结果:24只大鼠全部进入结果分析.缺血再灌注组明显高于假手术组(673.46±18.44),(224.71±10.58)nmol/L,(F=1 329.06,P＜0.01)],碱性成纤维细胞生长因子治疗组明显低于缺血再灌注组(378.37±21.08),(673.46±18.44)nmol/L(F=1 329.06,P＜0.01)].结论:碱性成纤维细胞生长因子能明显抑制大鼠缺血再灌注后脑组织内游离钙水平,起到稳定细胞膜,防止细胞内钙超载的作用.

Effect of basic fibroblast growth factor on rat brain intracellular free calcium following focal ischemia-reperfusion injury

BACKGROUND: Basic fibroblast growth factor (bFGF) possesses multiple functions such as promoting neuronal survival and growth of cell processes in vitro and antagonizing the toxicity of excitatory amino acids,thereby playing import roles in functional recovery of the central nervous system (CNS). But whether bFGF offers neuroprotection on ischemic brain tissues by modulating intracellular free calcium content remains unknown.OBJECTIVE: To explore the effect of bFGF on intracellular free Ca2+ in the neural cells in the event of focal cerebral ischemia-reperfusion (IR)injury.DESIGN: Randomized controlled study.SETTING: Department of Neurology of Second Hospital Affiliated to Zhengzhou University.MATERIALS: This study was conducted in the Laboratory of the Department of Neurology, Second Hospital Affiliated to Zhengzhou University between August and December 2003. Totally 24 SD were randomized into sham operation group, ischemic group, IR group and bFGF exposure group with 8 rats in each group.METHODS: Middle cerebral artery occlusion (MCAO) model was established in rats in IR group and bFGF exposure group by inducing arterial thrombosis with thread, which was not preformed in rats in the sham operation group. Rats in bFGF exposure group received intraperitoneal injection of 10 μg/kg bFGF immediately after ischemia,which was replaced by the same volume of physical saline in the other two groups. Free Ca2+ in brain cells was detected at 24 hours of IR.MAIN OUTCOME MEASURES: Free Ca2+ in the brain cells at 24hours of IR.RESULTS: All the 24 rats survived the experiment. Free Ca2+ in IR group was significantly higher than that of the sham operation group (673.46±18.44) vs (224.71±10.58) nmol/L, F=1 329.06, P ＜ 0.01], and also significantly higher in bFGF exposure group (378.37±21.08) nmol/L,F=1 329.06, P ＜ 0.01].CONCLUSION: Intracellular free calcium can be obviously depressed by bFGF following IR injury, which benefits cell membrane stability and help prevent intracellular Ca2+ overload.