| Objective: Recent years, many studies have discovered that ischemicpostconditioning (IP) could reduce the area of cerebral ischemia/reperfusion(I/R) injury though activating a variety of endogenous pathway to play a obviousneuroprotective effect. However, there were few studies on rapid and delayedremote ischemic postcondtioning (R/D-RIP) until now. So the purpose of ourresearch is going to prove whether rapid and delayed remote ischemicpostconditioning (R/D-RIP) has a neuroprotective effect or not by establishingstable90min Middle Cerebral Artery Occlusion (MCAO) model in rats and itsunderlying mechanisms. Method: Firstly, we established stable90min MiddleCerebral Artery Occlusion (MCAO) model in rats to prove the neuprotectiveeffects of rapid and delayed remote ischemic postconditioning (R/D-RIP).24male healthy Sprague Dawlay (SD) rats were randomly divided into three groups:⑴Control Group (n=8): the middle cerebral artery of rats was occludedfor90min, withdraw monofilament suture and then reperfused for48hours.⑵R-RIP Group (n=8): the middle cerebral artery of rats was occluded for90min,and the remote ischemic postconditioning was administered at the beginning ofreperfusion by withdrawing monofilament suture.⑶D-RIP Group: the middlecerebral artery of rats was occluded for90min, and the remote ischemicpostconditioning was administered at6hours after reperfusion by withdrawingmonofilament suture. The bilateral femoral arteries bluntly separated, at thebeginning of reperfusion or6hours after reperfusion, close/open them10min inturn for3circles by frog heart clip, namely remote ischemic postconditioning(RIP). Functional neurological outcome were measured at1hour after occlusion,12hours,24hours and48hours after reperfusion, respectively. At last rats weresacrificed at48hours after reperfusion, the paraffin-embedded tissue were takenand the infarct size were measured by HE stain. Secondly, In order to investigatethe underlying neuroprotective mechanism of rapid and delayed remoteischemic postconditioning (R/D-RIP) on ischemia and its differences. Weselected24male healthy SD rats and then randomly divided into4groups,6ratsper group:⑴Sham Group;⑵ControlGroup;⑶R-RIP Group;⑷D-RIP Group.Rats were sacrificed at48hours after reperfusion, then the specimens weretaken. We complete the relevant cell and molecular biology index detection.Results:⑴The infarct volume measured by HE staining show that compared with the control, R-RIP and D-RIP group were significantly smaller (P<0.05);moreover, the infarct volume of R-RIP group was also significantly smaller thanR-RIPC group (P<0.05).⑵The functional neurological score were tested at1hour after occlusion,12hour,24hours and48hours after reperfusion,respectively, and the results show that the score of R-RIP and D-RIP group weresignificantly higher than the control (P<0.05). The neurological score tested at1hour after occlusion,12hour,24hours after reperfusion of D-RIP group waslower than R-RIP group, but there were no significant different between the twogroups (P>0.05); however the neurological score tested at48hours afterreperfusion of D-RIP group were significantly lower than R-RIP group (P <0.05). Conclusions: Our results imply that both rapid and delayed remoteischemic postconditioning (R/D-RIP) could decrease the infarct volume ofischemia in rats, and improve the neurological score; moreover R-RIP groupcould decrease the infarct volume better and D-RIP group could improve theneurological score, especially at48hours after reperfusion. |
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