论文部分内容阅读
目的 探讨碱性成纤维细胞生长因子 (bFGF)对新生大鼠缺氧缺血性脑损伤 (HIBD)的防治作用及其机制。方法 将 6 3只 7日龄wistar大鼠分为 :假手术对照组 15只、HIBD组 18只和bFGF治疗组 30只 (17 5 μg/kg 12只 ,10 μg/kg 18只 )。制备大鼠HIBD模型 ,给予治疗组大鼠连续 7d腹腔注射bFGF ,对HIBD组腹腔注射等体积生理盐水作为对照 ,全部大鼠于术后 14d处死 ,观察脑的大体、光镜及电镜下的改变 ;另取鼠 72只 (bFGF组 12只 ,未治疗组 48只 ,对照组 12只 )制备HIBD模型 ,利用逆转录 聚合酶链式反应 (RT PCR)技术检测新生大鼠HIBD后不同时间脑皮质细胞间粘附分子 1(ICAM 1)mRNA的表达及bFGF干预对它的影响。结果 新生大鼠HIBD后 2周脑大体改变明显 ,脑萎缩、脑软化及空洞形成的发生率分别为 73 3%、6 0 0 %和 2 6 7%。bFGF治疗可降低脑萎缩、脑软化的发生率 (31 0 %、2 4 1% ) (P <0 0 5 )。电镜下可见bFGF对HIBD后的神经元、血管内皮细胞及神经胶质细胞的超微结构均有明显的促修复作用。HIBD 6h后 ,ICAM 1mRNA开始明显增高 ,2 4h达高峰 ,7d基本恢复至正常水平。高峰表达时病侧脑ICAM 1mRNA为正常组的 3 6倍 (P <0 0 1) ,为健侧脑的 2 2倍 (P <0 0 5 )。bFGF干预组ICAM 1mRNA表达低于HIBD组 (P <0 0
Objective To investigate the preventive and therapeutic effects of basic fibroblast growth factor (bFGF) on hypoxic-ischemic brain damage (HIBD) in neonatal rats and its mechanism. Methods Sixty-three 7-day-old Wistar rats were divided into sham operation control group (n = 15), HIBD group (n = 18) and bFGF treatment group (n = 30). HIBD model was established in rats. The rats in the treatment group were given intraperitoneal injection of bFGF for 7 consecutive days. The rats in HIBD group were injected intraperitoneally with equal volume of normal saline as control. All rats were sacrificed 14 days after operation. The changes of brain in general, light and electron microscopy ; Another 72 mice (bFGF group 12, untreated group 48, control group 12) prepared HIBD model, using reverse transcription polymerase chain reaction (RT PCR) technology to detect newborn rats HIBD at different times after cerebral cortex The Expression of Intercellular Adhesion Molecule 1 (ICAM 1) mRNA and the Effect of bFGF on It. Results HIBD in neonatal rats changed significantly after 2 weeks. The incidences of brain atrophy, cerebral softening and cavitation were 73 3%, 600% and 267%, respectively. bFGF treatment can reduce the incidence of cerebral atrophy and cerebral softening (31 0%, 214%) (P <0 05). Electron microscopy showed that bFGF had obvious pro-healing effects on the ultrastructure of neurons, vascular endothelial cells and glial cells after HIBD. After 6 h HIBD, ICAM 1 mRNA began to increase significantly, peaked at 24 h and returned to normal level on the 7th day. The ICAM 1 mRNA expression in diseased brain was 36% (P <0.01) higher than that in normal group at peak time, which was 2 2 times of that in healthy brain (P <0 05). The expression of ICAM 1mRNA in bFGF intervention group was lower than that in HIBD group (P <0 0)