中华神经医学杂志
中華神經醫學雜誌
중화신경의학잡지
CHINESE JOURNAL OF NEUROMEDICINE
2009年
4期
344-346
,共3页
宫利%王志%肖松华%刘运林%周海红%邢诒刚
宮利%王誌%肖鬆華%劉運林%週海紅%邢詒剛
궁리%왕지%초송화%류운림%주해홍%형이강
缺血后处理%局灶性脑缺血%神经保护%PI3K信号通路
缺血後處理%跼竈性腦缺血%神經保護%PI3K信號通路
결혈후처리%국조성뇌결혈%신경보호%PI3K신호통로
Ischemic postconditioning%Focal cerebral isehemia%Neuroprotection%Phosphoinositide 3-kinase signaling pathway
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.
目的 研究缺血後處理(IP)對腦缺血再灌註損傷的影響及其機製.方法 採用開顱機械閉塞法建立SD大鼠跼竈性腦缺血模型,通過開放/夾閉雙側頸總動脈實現IP.24隻大鼠按照隨機數字錶法分為IP組、非IP組、LY294002+IP組、DMSO+IP組,每組6隻,再灌註48 h後測腦梗死麵積;其中LY294002、DMSO于建模前1 h側腦室註入.結果 各組左側大腦皮層均可見清晰梗死竈,符閤血管分佈範圍.其中IP組腩梗死麵積(34.02%±7.17%)明顯小于非IP組(57.05%±10.05%),差異有統計學意義(P<0.05);LY294002+IP組腦梗死麵積(73.41%±2.06%)明顯大于DMSO+IP組(35.76%±1.51%),差異有統計學意義(P<0.05);DMSO+IP組與IP組腦梗死麵積差異無統計學意義(P>0.05).結論 IP可減輕跼竈性腦缺血大鼠的腦缺血再灌註損傷,PI3K信號通路參與其作用機製.
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.