| Objective:â‘ By detecting SOD activity and MDA content of the hippocampal tissue in SDrats to observe the protective effect of sevoflurane postcinditioning on cerebral ischemiareperfusion injury in rats.â‘¡By detecting heme oxygenase-1 (HO-1) content of thehippocampal tissue in SD rats to investigate the effects of sevoflurane postconditioning on hemeoxygenase-1 expression and the protection mechanisms of sevoflurane postconditioning oncerebral ischemia-reperfusion injury in rats.Methods: Forty adult male Sprague-Dawley (SD) rats of clean grade weighing 230-270 g wererandomly assigned to five groups, and every group was 8 rats. Sham operation group (group C):separated both sides of the common carotid artery and right jugular vein, and exposed for 20minutes, then 5 minutes before suturing the wound for endotracheal intubation in rats, inhalationoxygen 15 minutes, put the rats back in. The rats in other four groups were made models ofcerebral ischemia reperfusion injury. The occlusion of bilateral carotid arteries of 20 minutescombined with hypotension method to establish the model of cerebral ischemia. Ischemia andreperfusion group (group I/R): made cerebral ischemia-reperfusion model, before reperfusion 5minutes tracheal intubation for rats, inhalation oxygen 15 minutes; Ischemia andreperfusion+2.5% sevoflurane group (group S): before reperfusion 5 minutes tracheal intubationfor rats, inhalation 2.5% sevoflurane 15 minutes; Znpp+I/R model+2.5% sevoflurane group(group S+Z): before mading model by femoral vein injected specificity inhibitors Znpp of HO-110 mg/kg (dissolved in DMSO 0.5 ml), the remaining operation with the S group; AndDMSO+I/R model+2.5% sevoflurane group (group S+D): before mading model by femoral veininjected DMSO 0.5 ml, the remaining operation with the S group. After reperfution 24 hours, allof the rats were sacrificed and the hippocampus were got. Under light-microscopy pathologicalchanges of every group hippocampus were observed, and SOD activity, MDA and HO-1 contentwere detected.Results:â‘ Compared with C group, in other four groups the SOD activity was significantlydecreased (P<0.05), and MDA was significantly increased (P<0.05); compared with I/R group,in S and S+D group SOD activity was significantly high (P<0.05), and MDA was significantlylower (P<0.05), between S+Z and I/R group there is not statistically significant in SOD activityand MDA differences (P>0.05); between S and S+D group there is not statistically significant inSOD activity and MDA differences (P>0.05).â‘¡Immunohistochemical method showed:compared with C group, between S+Z and C group there is not statistically significant in HO-1 difference (P>0.05), in the other three groups of HO-1 significantly increased (P<0.05);compared with I/R group, S+Z group of HO-1 was significantly lower (P<0.05), in group S andS+D group of HO-1 significantly increased (P<0.05); between S and S+D group there is notstatistically significant in HO-1 difference (P>0.05).â‘¢Under the light microscope, in S andS+D group pathology of hippocampal damage reduced comparing with that in I/R and S+Zgroup.Conclusion:â‘ Cerebral ischemia and reperfusion injury can induce HO-1 to express.â‘¡Sevoflurane can partly increase the expression of HO-1 to reduce oxidative stress andpathological changes.â‘¢The protective effect of sevoflurane may be blocked by a specificinhibitor Znpp of HO-1, which suggests that cerebral protective effect of sevofluranepostconditioning mediated by HO-1. |
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