Effects of exogenous bFGF on glial fibrillary acidic pro tein expression in neonatal rat brain with hypoxic-ischemic brain damage
Hua Wang
Abstract
Hua Wang
Abstract
Objective: To investigate the effect of hy po xia-ischemia on glial fibrillary acidic protein (GFAP) and endogenous basic fib roblast growth factor (bFGF), and the effect of exogenous bFGF on GFAP expressio n in hypoxic-ischemic brain of neonatal rats. Methods: Expres sions of GFAP and endogenous bFGF were examined with immunohistochemical stainin g and image quantitative analysis. Results: Expression of GFAPwas weak in rats 7 days after birth and reached peak 14 days after birth, and w as major in cerebral white matter. The expression of GFAP was also detected in t he hippocampus and cerebral white matter 28 days after birth. The expression ofGFAP increased after hypoxia-ischemia and reached peak 48 hours after hypoxia- ischemia. Exogenous bFGF enhanced the expression of GFAP, and the effect was themost 24 hours after bFGF delivery and persistent to 5 days. Endogenous bFGF cou ld be detected in the brain of normal neonatal rats, which was most abundantly e xpressed 10 days after birth. Distribution of bFGF was similar to that of GFAP.Conclusion: Exogenous bFGF could enhance expression of GFAP inhypoxic-ischemic brain of neonatal rat, which may play important roles in rest oration of neurons damaged by hypoxia-ischemia.
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Objective: To investigate the effect of hy po xia-ischemia on glial fibrillary acidic protein (GFAP) and endogenous basic fib roblast growth factor (bFGF), and the effect of exogenous bFGF on GFAP expressio n in hypoxic-ischemic brain of neonatal rats. Methods: Expres sions of GFAP and endogenous bFGF were examined with immunohistochemical stainin g and image quantitative analysis. Results: Expression of GFAPwas weak in rats 7 days after birth and reached peak 14 days after birth, and w as major in cerebral white matter. The expression of GFAP was also detected in t he hippocampus and cerebral white matter 28 days after birth. The expression ofGFAP increased after hypoxia-ischemia and reached peak 48 hours after hypoxia- ischemia. Exogenous bFGF enhanced the expression of GFAP, and the effect was themost 24 hours after bFGF delivery and persistent to 5 days. Endogenous bFGF cou ld be detected in the brain of normal neonatal rats, which was most abundantly e xpressed 10 days after birth. Distribution of bFGF was similar to that of GFAP.Conclusion: Exogenous bFGF could enhance expression of GFAP inhypoxic-ischemic brain of neonatal rat, which may play important roles in rest oration of neurons damaged by hypoxia-ischemia.
Key concepts: Glial fibrillary acidic protein, Ischemia, Hypoxia (environmental), Endogeny, Immunohistochemistry, Endocrinology, Basic fibroblast growth factor, Internal medicine