ABSTRACT
We investigate the expression of basic fibroblast growth factor (bFGF) during ischemia-reperfusion with or without electroacupuncture (EA) treatment, and observe the effect of EA on ischemic cerebral injury. In the present study, a sensitive sandwich time-resolved fluoroimmunoassay (TR-FIA) method was developed to quantitatively analyze the levels of bFGF in rat brain. The results indicated that the obvious cerebral infarction and swelling were observed after ischemia-reperfusion, and the opening amount of cerebral blood micrangium was increased. In the meantime, the expression of bFGF was also improved in striatum and frontoparietal cortex. EA alleviated the ischemic injuries induced by MCAO and markedly upregulated the opening amount of the micrangium. Owing to application of EA, the expression of bFGF was notably enhanced in striatum and cortex. The results give us some hints for the neuroprotective mechanism of EA, that is, EA may partially exert protective effects on neurons through regulating the blood dynamics and the endogenous expression of bFGF.
Subject(s)
Brain Ischemia/metabolism , Brain Ischemia/therapy , Brain/metabolism , Fibroblast Growth Factor 2/metabolism , Animals , Brain/pathology , Brain/physiopathology , Brain Ischemia/physiopathology , Electroacupuncture , Fluorescence Polarization Immunoassay , Male , Nerve Tissue Proteins/metabolism , Rats , Rats, Sprague-Dawley , Treatment OutcomeABSTRACT
The present study was designed to investigate whether the Electroacupuncture (EA) is beneficial to extenuate cerebral injuries following transient Middle Cerebral Artery Occlusion (MCAO), as well as to observe the effect of EA on expression of Basic Fibroblast Growth Factor (bFGF) -like Immunoreactivity (IR) in rat brains. The results indicate that gross neuronal damages include infarction, swelling and neuron loss, accompanied by increased bFGF-like IR expression following MCAO. In peri-infarct striatum, bFGF-like IR was mainly located in astrocytes except some neurons also showed an upregulation of the IR; in frontoparietal cortex, strong induction of bFGF-like IR was mostly seen in neurons. Both the EA applied during ischemia and reperfusion could evidently alleviate cerebral lesion extent, notably upregulate the expression of bFGF-like IR in striatum and cortex, but there was no significant difference between the effects of EA applied during ischemia and reperfusion, except EA applied during reperfusion seems to be more effective in reducing the cerebral swelling. The results implied that, in striatum, astrocytes might play an important role in the protection of neuron via the expression of bFGF; whereas in cortex, neurons may exert autoprotection through secreting bFGF themselves. One possible protective effect of EA lies in regulating the endogenous expression of bFGF.