Mechanisms and neuro-protective effect of basic fibroblast growth factor on brain injury following global ischemia-reperfusion in rabbits
LI Jiaoku
Abstract
LI Jiaoku
Abstract
Objective To study the mechanisms and neuroprective effects of basic fibroblast growth factor(bFGF) on brain injury following global ischemia-reperfusion.Methods Twenty-four rabbits were randomly divided into three groups. Brain injury following global ischemia-reperfusion was induced by ligationof four vessels and systemic hypotension. bFGF was intravenously infused after reperfusion in bFGF group (Group C). The same volume of normal saline was applied in control group (Group B), only dissection of four vessels performed in sham group (Group A). Blood samples were taken for determination of serum neuron specific enolase (NSE), S-100B, tumor necrosis factor-α(TNF-α), interleukin-1 (IL-1), interleukin-8 (IL-8) at baseline and 0.5, 1, 3, 6 h after reperfusion. Brain water was measured by dry-wet weight method and pathological features were examined. Results Serum NSE and S-100 were increased at 1 h after reperfusion and reached their peaks at 6 h after reperfusion, but were higher in group B than those in group C at 3 h and 6 h after reperfusion. TNF-α was increased in group B and group C after ischemia, then continuously rose together with IL-1,IL-8 and reached their peaks at 6 h after reperfusion. TNF-α and IL-1 in group C were lower than those in group B at 3 h and 6 h. IL-8 and brain water were not different between group B and group C. There were milder pathological changes in group C.Conclusions bFGF protects brain from injury following global ischemia-reperfusion, by reducing production of inflammatory factors and antagonizing their adverse effects.
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Objective To study the mechanisms and neuroprective effects of basic fibroblast growth factor(bFGF) on brain injury following global ischemia-reperfusion.Methods Twenty-four rabbits were randomly divided into three groups. Brain injury following global ischemia-reperfusion was induced by ligationof four vessels and systemic hypotension. bFGF was intravenously infused after reperfusion in bFGF group (Group C). The same volume of normal saline was applied in control group (Group B), only dissection of four vessels performed in sham group (Group A). Blood samples were taken for determination of serum neuron specific enolase (NSE), S-100B, tumor necrosis factor-α(TNF-α), interleukin-1 (IL-1), interleukin-8 (IL-8) at baseline and 0.5, 1, 3, 6 h after reperfusion. Brain water was measured by dry-wet weight method and pathological features were examined. Results Serum NSE and S-100 were increased at 1 h after reperfusion and reached their peaks at 6 h after reperfusion, but were higher in group B than those in group C at 3 h and 6 h after reperfusion. TNF-α was increased in group B and group C after ischemia, then continuously rose together with IL-1,IL-8 and reached their peaks at 6 h after reperfusion. TNF-α and IL-1 in group C were lower than those in group B at 3 h and 6 h. IL-8 and brain water were not different between group B and group C. There were milder pathological changes in group C.Conclusions bFGF protects brain from injury following global ischemia-reperfusion, by reducing production of inflammatory factors and antagonizing their adverse effects.
Key concepts: Medicine, Basic fibroblast growth factor, Reperfusion injury, Ischemia, Enolase, Saline, Anesthesia, Tumor necrosis factor alpha