The Effects Of Sodium Ferulate On Glial Fibrillary Acidic Protein Of Astrocyte After Forebrain Ischemia-Reperfusion Of Rats

Cerebrovascular disease do great harm to human's heath,which hasbeen one of the important reasons leading to disability and death at present. Cerebral ischemia reperfusion has become the key in the clinical therapy of ischemic cerebrovascular disease(ICD). The astrocyte (Ast) , the maximum quantity in the central nervous system (CNS), is a kind of spongiocytes and composes of approximately 40% of the total cells in an aldult'sCNS. Ast plays a complex role in Cerebral ischemia reperfusion.Glial fiber acid protein( GFAP) is the sign of astrocytes,which is always used as an index of active state of Asts. Up to now ,endothelin is the strongest vasoconstrictor which was discovered. And its damage on cerebral ischemia has been identified. In recent years, endothelin receptor (ETR) has been discovered in Asts and also generated by active Asts,which aggravates ischemia lesion. Sodium ferulate is a receptor antagonist of ET,which can antagonize vessel constriction to reduce ischemic damages. It has never been reported whether sodium ferulate canantagonize ETR in Asts to regulate Asts' activation and whether it has the protective effects on the brain.This experiment estabished a forebrain reperfusion model of mice, to observe the influences that different brain tissues' pathological morphology changes and GFAP 's expression in Ast by using sodium ferulate. The result showedin HE staining is that neuronsand the neuroglia cells were in the normal appearance in the sham operated group,no hydropsia in mesenchyma;in the controlgroup hydropsia appeared in the brain tissue,some neurons and neuroglia cells experienced degeneration and necrosis,spongiocyte's proliferation could been seen as time going. In some specimens there were many round or oval-shap,kytoplasm-abundant Ast proliferating, eosinophilic color,whose nucleuswas small,compact and unilateral. While in the therapy group,hydropsia ofbrain tissue,neuon necrosis and astrocyte's proliferation were lessened.GFAP immunohistochemistry showed that, in the sham operated group, afew GFAP expressions could been seen in Ast with thin cell volumes and neurodendrons;in the control group Ast's expressions increased obviously, withbig cell volumes and neurodendrons,and with GFAP expression immunopositive(P<0.05). The results revealed that Ast proliferated reactively after ischemia, while sodium ferulate treatment group compared with the sham operated group and control group at different time, GFAP's immunopositive expressions were situated between the two groups (P<0.05).The experiment above confirmes that sodium ferulate can antagonize ETBon Ast and displays protective function. ET is a biological peptide which is composed of 21 amino acids produced by endothelial cells. Through biological effect with the corresponding endothelin receptor,ETB receptor are mainly expressed by Ast in CNS ,therefore the astrocyte has been regarded as ET target cell. Ischemia cause ET to increase and act uponETB receptor and induce astrocyte activiation. The active astrocyte can release glutanic acid and promote neuron cells degenerating. Sodium ferulate is the major component of traditional Chinese medicine chuanxiong and is a non-peptide ETR antagonist. Its chemical name is 3-methoxy -4-hydroxyl -cinnamic acid sodium. Massive fundamental and clinical researches prove that its phenol-hydroxy structure eliminates free radical and its benzol-alkene structure antagonizes ETto protecte blood vessel endothelium and adjust Vasomotor function.The significance of the experiment is to provide sufficient experimental evidence for its clinical application in treating ischemic cerebrovascular disease. Through mice' repeatedly cerebral ischemia reperfusion, we simulate cerebral ischemia of human being and observe GFAP's expression in Asts after the reperfusion and the intervention of sodium ferulate,we illustrates that ETR antagonist-sodium ferulate not only relieves vasoconstriction and protects ischemic damage,but also regulates Ast's activation and protects the brain, In the subsequent experiments and clinical works, we will discuss the distictions of different concertrations of sodium ferulate acting upon Ast after ischemia and approach the mechanism of interaction further. Still we will discuss Ast's function deeply and search for its new therapy strategy,not only displaying neuroprotective effect of Ast, but also suppressing its nerve toxicity. That will become a topic of great significance.