Peng Hao, Zhou Hong, Xiong Ying
Department of Pediatrics, West China Second Hospital, Sichuan University, Chengdu 610041, China.
Zhongguo Dang Dai Er Ke Za Zhi. 2006 Jun;8(3):235-8.
Basic fibral growth factor (bFGF) might have a role in the restoration and regeneration of injured neurons following hypoxic-ischemic brain damage (HIBD), but its mechanism has not been fully elucidated. Nestin is an intermediate filament protein expressed in dividing cells during the early stages of CNS development, but it can be reinduced in adults during regeneration of injured neurons after CNS injury. This study investigated the effect of exogenous bFGF on nestin expression in neonatal rats following hypoxia-ischemia (HI) and to explore the possible mechanism.
Eighty-four 7-day-old SD rats were randomly assigned into a Sham-operation group, a HIBD group and a bFGF intervention group (n=28 each). HIBD was induced by ligation of the left carotid artery along with 8% oxygen exposure in neonatal rats from the latter two groups. The Sham-operation group was not subjected to HI. The bFGF intervention group received an intraperitoneal injection of bFGF daily (4000 U/kg). Each group was randomly subdivided into groups sacrificed immediately, at 3, 12 and 24 hrs and 3, 7 and 14 days after HI (n=4). The expression of nestin in the cerebral cortex, hippocampus and extraventricular zone was examined with immunohistochemical staining and image quantitative analysis.
Nestin was weakly expressed in the hippocampus and extraventricular zone and not expressed in the cortex in the Sham-operation group. The nestin in the cortex, hippocampus and extraventricular zone was significantly increased after HIBD, peaking at 7 days. bFGF treatment increased the nestin expression in the cortex, hippocampus and extraventricular zone and statistical differences were observed from 1 to 14 days after HI when compared with the untreated HIBD group.
Exogenous bFGF can up-regulate the nestin expression in neonatal rats following HIBD. The effects of restoration and regeneration of bFGF on injured neurons may be associated with increased nestin expression in neonatal rats.
碱性成纤维细胞生长因子(bFGF)可能在缺氧缺血性脑损伤(HIBD)后受损神经元的修复和再生中发挥作用,但其机制尚未完全阐明。巢蛋白是一种中间丝蛋白,在中枢神经系统(CNS)发育早期的分裂细胞中表达,但在成年中枢神经系统损伤后受损神经元再生过程中可再次诱导表达。本研究探讨外源性bFGF对新生大鼠缺氧缺血(HI)后巢蛋白表达的影响,并探索其可能机制。
84只7日龄SD大鼠随机分为假手术组、HIBD组和bFGF干预组(每组28只)。后两组新生大鼠通过结扎左颈动脉并暴露于8%氧气诱导HIBD。假手术组未进行HI处理。bFGF干预组每天腹腔注射bFGF(4000 U/kg)。每组随机再分为HI后立即处死组、3小时、12小时和24小时处死组以及3天、7天和14天处死组(每组4只)。采用免疫组织化学染色和图像定量分析检测大脑皮质、海马和脑室下区巢蛋白的表达。
假手术组海马和脑室下区巢蛋白表达较弱,皮质未表达。HIBD后大脑皮质、海马和脑室下区的巢蛋白明显增加,在7天时达到峰值。与未处理的HIBD组相比,bFGF处理增加了大脑皮质、海马和脑室下区的巢蛋白表达,在HI后1至14天观察到统计学差异。
外源性bFGF可上调新生大鼠HIBD后的巢蛋白表达。bFGF对受损神经元的修复和再生作用可能与新生大鼠巢蛋白表达增加有关。