Expression Of Hsp22 And VEGF After Brain I/R Injury In Gerbils And Neuroprotective Effects Of Them

Object: In this study we investigated the expression and protective mechanisms of Hsp22 and VEGF in brain tissue following cerebral ischemic reperfusion in gerbils and whether they are correlative.Method:(1) Animal Groups: forty five gerbils were randomly divided into there groups: Normal Group (n=5), Sham-operated Group, Ischemia-Reperfusion Group(I/R). Sham-operated Group and I/R Group are divided into four subgroups (each group has five animals): 6 hours group, 1day group, 3days group, 7days group.(2) Mode: Each subject except normal group was anesthetized with 3% pentobarbital(30mg/kg,ip, then a midline incision was made in the neck and surgical silk was loosely placed around both sides isolated commom carotid arteries. A traumatic miniature aneurysm clips were attached to occlude both carotid arteries for 10 min. At the end of the occlusion period, blood flow was reestablished. In sham-operated group, the arteries were exposed but not occluded. The wound was then sutured, and the animals were allowed to recover. The animals were sacrifice by decapitation at correspondence time.(3) Histological analysis of tissue injury: staining with stained with haematoxylin and eosin haematoxylin and eosin (HE).(4) Immunohistochemical Methods.(5) Experimental results were analyzed with the statistic soft package of Spss15.0Result:(1)Staning with HE: The tissues of normal group and sham-operated group was integrate ,but that of I/R were changed with gliocyte hyperplasia and hypertrophia, interstitial edema, cellular edema, gliocyte and neuron edema, neuron necrosis.(2) Immunohistochemical Methods: The normal group and sham-operated group was measured low Hsp22 and VEGF, We measured the overexpression of Hsp22 and VEGF 6 hours after I/R, with peak expression at 3days ,but appeared to decline by 7 days and there was significance between groups(p<0.05). The data presented herein provide a positive correlation between expression of Hsp22, resist to stress and expression of VEGF, mediate the transcriptional activation of hypoxia-responsive genes.Conclusions:(1) We report that the expression of Hsp22 was increased after gerbils brain I/R injury and can exert neuroprotective effects.(2) Expression of VEGF was upregulated and can exert neuroprotective effects following gerbils cerebral ischemic reperfusion.(3) There was a positive correlation between expression of Hsp22 and expression of VEGF after gerbils brain I/R injury.