CAJ | 학술논문

目的研究缺血后处理(IP)对脑缺血再灌注损伤的影响及其机制.方法采用开颅机械闭塞法建立SD大鼠局灶性脑缺血模型,通过开放/夹闭双侧颈总动脉实现IP.24只大鼠按照随机数字表法分为IP组、非IP组、LY294002+IP组、DMSO+IP组,每组6只,再灌注48 h后测脑梗死面积;其中LY294002、DMSO于建模前1 h侧脑室注入.结果各组左侧大脑皮层均可见清晰梗死灶,符合血管分布范围.其中IP组腩梗死面积(34.02%±7.17%)明显小于非IP组(57.05%±10.05%),差异有统计学意义(P＜0.05);LY294002+IP组脑梗死面积(73.41%±2.06%)明显大于DMSO+IP组(35.76%±1.51%),差异有统计学意义(P＜0.05);DMSO+IP组与IP组脑梗死面积差异无统计学意义(P＞0.05).结论 IP可减轻局灶性脑缺血大鼠的脑缺血再灌注损伤,PI3K信号通路参与其作用机制.
목적 연구결혈후처리(IP)대뇌결혈재관주손상적영향급기궤제.방법 채용개로궤계폐새법건립SD대서국조성뇌결혈모형,통과개방/협폐쌍측경총동맥실현IP.24지대서안조수궤수자표법분위IP조、비IP조、LY294002+IP조、DMSO+IP조,매조6지,재관주48 h후측뇌경사면적;기중LY294002、DMSO우건모전1 h측뇌실주입.결과 각조좌측대뇌피층균가견청석경사조,부합혈관분포범위.기중IP조남경사면적(34.02%±7.17%)명현소우비IP조(57.05%±10.05%),차이유통계학의의(P＜0.05);LY294002+IP조뇌경사면적(73.41%±2.06%)명현대우DMSO+IP조(35.76%±1.51%),차이유통계학의의(P＜0.05);DMSO+IP조여IP조뇌경사면적차이무통계학의의(P＞0.05).결론 IP가감경국조성뇌결혈대서적뇌결혈재관주손상,PI3K신호통로삼여기작용궤제.
Objective To investigate the neuroprotective effect of ischcmic posteonditioning (IP)against cerebral ischemia-reperfusion injury and the role of phosphoinositide 3-kinase(P13K)signaling pathway in the neuroprotection. Methods Focal cerebral ischernia was induced in 24 SD rats by permanent distal middle cerebral artery occlusion and transient bilateral comlllOn carotid artery occlusion.The rats were then randomized into 4 groups for treatment with IP,LY294002+IP,DMSO+IP,or without IP.In LY294002+IP and DMSO+IP groups,LY294002 or DMSO was injcoted into the ventricular space on the ischemic side 1 h before ischemia.The cerebral infarct sizes wgre measured in all the 4 groups at 48h after the reperfusion.Results Cerebral infarcts were observed in all the groups on theischemic side,all locating in the left neocortex and the middle cerebral artery territory.At48h after reperfusion,the infarct size was significantly smaller in rats with IP(34.02%±7.17%)than in those without IP(57.05%±10.05%)(P＜0.05),and significantly larger in LY294002+IP group(73.41%±2.06%)than in DMSO+IP group(35.76%±1.51%)(P＜0.05).No significant difference was found in the infarctsize between DMSO+IP group and IP group(P＞0.05).Conclusion IP ameliorates cerebral reperfusion mjury in rats,and the mechanism of this neuroprotective effect involves the preservation of PI3K activity.