Effects and mechanism of basic fibroblast growth factor on hypoxic-ischemic brain damage in neonatal rats

Objective To investigate the protective effects and mechanism of basic fibroblast growth factor (bFGF) on hypoxic ischemic brain damage (HIBD) in neonatal rats.Methods HIBD model was established in 63 wistar rats of 7 day old, the macro and micro morphological features in HIBD rats treated with bFGF were compared with those in HIBD rats without the treatment of bFGF. Intercellular adhesion molecule 1 (ICAM 1) mRNA in the bilateral cortex was detected at different times in HIBD rats by reverse transcription polymerase chain reaction (RT PCR). The levels of ICAM 1 mRNA in HIBD rats treated with bFGF were also measured. Results Two weeks after hypoxic ischemia (HI), the brain tissue at the carotid ligation lateral of neonatal rats showed severe injury. The incidences of brain atrophy, malacia and cavitation were 73.3%, 60 0% and 26.7%, respectively. The treatment with bFGF could greatly relieve the cerebral injury of HI, and reduce the incidences of brain atrophy and malacia to 31 0% and 24.1%, respectively ( P 0.05). The ultra structures of neurons, endothelial cells and glia in hippocampus also degenerated greatly following HI, while it could be relieved with the treatment of bFGF when compared with the control group. The expression of ICAM 1 mRNA increased markedly 6 h after HI, reached the peak level at the 24th h, and returned to the normal level at the 7th day. The maximum expression of ICAM 1 mRNA was 3.6 times higher at the ischemic cortex in HIBD rats than that in normal rats ( P 0 01), and 2.2 times higher at the ischemic side than that at the nonischemic area ( P 0 05). The level of ICAM 1 mRNA in HIBD rats treated with bFGF reduced significantly than that in HIBD rats without the treatment of bFGF ( P 0 05).Conclusion bFGF appeared globally neuroprotective effects on the developing brain in a neonatal model of HIBD, its mechanism might be associated with promoting the recovery of the neurons and suppressing the over expression of ICAM 1 following HIBD.