Effect of Qi-tonifying and Stasis-eliminating Therapy (益气活血法)on Expression of Vascular Endothelial G

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Objective:To investigate the effects and mechanism of qi-tonifying and stasis eliminating(QTSE)therapy on the expression of vascular endothelial growth factor(VEGF)and its receptors Fit-1 and Fik-1 in the brains of intracerebral hemorrhagic(model)rats.Methods:One hundred and eighty Sprague-Dawley rats were randomly divided into six groups:the normal group (n=5),the sham-operative(SO)group(n=35),the model group(n=35),the QTSE group(n=35),the QT group(n=35)and the SE group(n=35).All the rats except those in the normal group and SO group were established into an intracerebral hemorrhage(ICH)model by intracerebral injection of collagenase type Ⅶ and the latter three were orally administered with Buyang Huanwu Decoction (补阳还五汤,a classical recipe for QTSE)or with some of its components for qi-tonification and for stasis-elimination,respectively.To the other three groups,normal saline solutions were given instead.Behavioral tests were carried out in the animals randomly chosen from each group on days 1,2,4,7,14,21 and 28 after modeling.The expressions of VEGF,Fik-1 and Fit-1 were determined by immunohistochemistry and the number of vascular segments with positive expression in the injured brain area of the rats was calculated.Results,From day 7 onwards,the asymmetric forelimb use rate in the QTSE group recovered more significantly than that in the other model groups.In the model group,the expressions of VEGF,Fik-1 and Fit-1 appeared on day 1 and reached a peak on day 21,then weakened gradually.In the QTSE group,as compared with the other model groups,a higher level of VEGF expression was shown from day 7(P<0.01)and a higher level of Fit-1 expression was shown from the 7th day to the 21st day(P<0.01).Conclusion:QTSE therapy can up-regulate the expressions of VEGF and its receptors(Flk-1 and Fit-1)and improve the recovery of kinetic function in the ICH rats,which may be correlated with its action in modulating vascular regeneration to promote the reconstruction of microvascular networks in the damaged areas.
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