中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2012年
9期
1130-1132
,共3页
刘孝洁%时飞%毕燕琳%陈怀龙%李颖%王明山
劉孝潔%時飛%畢燕琳%陳懷龍%李穎%王明山
류효길%시비%필연림%진부룡%리영%왕명산
低温,人工%热休克蛋白类%再灌注损伤%脑%老年人
低溫,人工%熱休剋蛋白類%再灌註損傷%腦%老年人
저온,인공%열휴극단백류%재관주손상%뇌%노년인
Hypothermia,induced%Heat-shock proteins%Reperfusion injury%Brain%Aged
目的 探讨亚低温对短暂性脑缺血再灌注老龄大鼠海马葡萄糖调节蛋白78(GRP78)表达的影响.方法 健康雄性老龄SD大鼠144只,体重450~550 g,采用随机数字表法,将其随机分为3组(n=48):假手术组(S组)、脑缺血再灌注组(I/R组)、全身亚低温组(H组).采用四血管阻断法建立全脑缺血再灌注模型,脑缺血5 min再灌注.H组于再灌注即刻向大鼠全身喷洒酒精行体表降温,维持直肠温32~34℃3h.分别于再灌注6、12、24、48 h时,采用免疫组织化学方法和Western blot法测定海马GRP78的表达;HE染色法计数海马存活神经元数目.结果 与S组相比,I/R组再灌注各时点海马存活神经元计数降低,再灌注6、12、24 h时海马GRP78表达上调,再灌注48 h时表达下调,H组再灌注各时点海马存活神经元计数降低,海马GRP78表达上调(P<0.05);与I/R组相比,H组再灌注12、24和48 h时海马存活神经元计数升高,再灌注各时点GRP78表达上调(P<0.05).结论 亚低温可进一步上调老龄大鼠短暂性脑缺血再灌注时海马GRP78的表达,从而减轻内质网应激反应,减轻脑损伤.
目的 探討亞低溫對短暫性腦缺血再灌註老齡大鼠海馬葡萄糖調節蛋白78(GRP78)錶達的影響.方法 健康雄性老齡SD大鼠144隻,體重450~550 g,採用隨機數字錶法,將其隨機分為3組(n=48):假手術組(S組)、腦缺血再灌註組(I/R組)、全身亞低溫組(H組).採用四血管阻斷法建立全腦缺血再灌註模型,腦缺血5 min再灌註.H組于再灌註即刻嚮大鼠全身噴灑酒精行體錶降溫,維持直腸溫32~34℃3h.分彆于再灌註6、12、24、48 h時,採用免疫組織化學方法和Western blot法測定海馬GRP78的錶達;HE染色法計數海馬存活神經元數目.結果 與S組相比,I/R組再灌註各時點海馬存活神經元計數降低,再灌註6、12、24 h時海馬GRP78錶達上調,再灌註48 h時錶達下調,H組再灌註各時點海馬存活神經元計數降低,海馬GRP78錶達上調(P<0.05);與I/R組相比,H組再灌註12、24和48 h時海馬存活神經元計數升高,再灌註各時點GRP78錶達上調(P<0.05).結論 亞低溫可進一步上調老齡大鼠短暫性腦缺血再灌註時海馬GRP78的錶達,從而減輕內質網應激反應,減輕腦損傷.
목적 탐토아저온대단잠성뇌결혈재관주노령대서해마포도당조절단백78(GRP78)표체적영향.방법 건강웅성노령SD대서144지,체중450~550 g,채용수궤수자표법,장기수궤분위3조(n=48):가수술조(S조)、뇌결혈재관주조(I/R조)、전신아저온조(H조).채용사혈관조단법건립전뇌결혈재관주모형,뇌결혈5 min재관주.H조우재관주즉각향대서전신분쇄주정행체표강온,유지직장온32~34℃3h.분별우재관주6、12、24、48 h시,채용면역조직화학방법화Western blot법측정해마GRP78적표체;HE염색법계수해마존활신경원수목.결과 여S조상비,I/R조재관주각시점해마존활신경원계수강저,재관주6、12、24 h시해마GRP78표체상조,재관주48 h시표체하조,H조재관주각시점해마존활신경원계수강저,해마GRP78표체상조(P<0.05);여I/R조상비,H조재관주12、24화48 h시해마존활신경원계수승고,재관주각시점GRP78표체상조(P<0.05).결론 아저온가진일보상조노령대서단잠성뇌결혈재관주시해마GRP78적표체,종이감경내질망응격반응,감경뇌손상.
Objective To investigate the effect of mild hypothermia on glucose regulated protein 78 (GRP78) expression in hippocampus following transient cerebral ischemia-reperfusion (I/R) in aged rats.Methods One hundred and forty-four male aged Sprague-Dawley rats,weighing 450-550 g,were randomly divided into 3 groups (n=48 each): sham operation group (group S),I/R group and mild hypothermia group (group H).Global cerebral I/R was induced by 4-vessel occlusion method.Bilateral vertebral arteries were permanently occluded by cauterization,and bilateral carotid arteries were occluded for 5 min.The surface cooling was started immediately after reperfusion and maintained for 3 h.During surface cooling,the body temperature was maintained at 32-34 ℃(rectal).At 6,12,24 and 48 h of reperfusion,the expression of GRP78 was determined using immuno-histochemisty and Western blot,and the viable neurons in CA1 area were counted.Results The number of viable neurons was significantly smaller at each time point,and the expression of GRP78 was significantly higher at 6,12 and 24 h of reperfusion,while lower at 48 h of reperfusion in I/R group,and the number of viable neurons was significantly smaller,and the expression of GRP78 was significantly higher at each time point in group H than in group S (P< 0.05).The number of viable neurons was significantly larger at 12,24 and 48 h of reperfusion,and the expression of GRP78 was significantly higher at each time point in group H than in group I/R (P < 0.05).Conclusion Mild hypothermia can further up-regulate GRP78 expression in hippocampus following transient cerebral I/R in aged rats,thus reducing endoplasmic reticulum stress and cerebral I/R injury.