中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2013年
4期
493-495
,共3页
张小玲%薛荣亮%王海丽%党莎杰%吕建瑞%吴刚%雷晓鸣%李伟%何家璇
張小玲%薛榮亮%王海麗%黨莎傑%呂建瑞%吳剛%雷曉鳴%李偉%何傢璇
장소령%설영량%왕해려%당사걸%려건서%오강%뢰효명%리위%하가선
脂氧素类%再灌注损伤%脑%细胞凋亡%后处理
脂氧素類%再灌註損傷%腦%細胞凋亡%後處理
지양소류%재관주손상%뇌%세포조망%후처리
Lipoxins%Reperfusion Injury%Brain%Apoptosis%Postconditioning
目的 评价脂氧素A4时处理对大鼠全脑缺血再灌注时细胞凋亡的影响.方法 雄性成年SD大鼠180只,体重200 ~ 250 g,采用随机数字表法,将其分为3组:假手术组(S组)、缺血再灌注组(I/R组)和脂氧素A4后处理组(L组).I/R组和L组采用四血管阻塞法建立大鼠全脑缺血再灌注损伤模型.L组于再灌注即刻侧脑室注射脂氧素A4 100 ng(用生理盐水稀释至5ul),S组和I/R组侧脑室注射生理盐水5ul.分别于再灌注2、6、12、24和72 h时,处死6只大鼠,取脑组织,行HE染色,光镜下观察病理学结果,采用免疫组化法测定海马CA1区caspase-3表达.分别于再灌注2、6、12、24和72 h时,处死6只大鼠,取海马组织,采用流式细胞仪检测细胞凋亡率.结果 与S组比较,I/R组和L组再灌注各时点海马CA1区caspase-3表达上调,海马组织细胞凋亡率升高(P<0.01);与I/R组比较,L组再灌注各时点海马CA1区caspase-3表达下调,海马组织细胞凋亡率降低(P<0.01),病理学损伤减轻.结论脂氧素A4后处理减轻大鼠全脑缺血再灌注损伤的机制与下调caspase-3表达,减少细胞凋亡有关.
目的 評價脂氧素A4時處理對大鼠全腦缺血再灌註時細胞凋亡的影響.方法 雄性成年SD大鼠180隻,體重200 ~ 250 g,採用隨機數字錶法,將其分為3組:假手術組(S組)、缺血再灌註組(I/R組)和脂氧素A4後處理組(L組).I/R組和L組採用四血管阻塞法建立大鼠全腦缺血再灌註損傷模型.L組于再灌註即刻側腦室註射脂氧素A4 100 ng(用生理鹽水稀釋至5ul),S組和I/R組側腦室註射生理鹽水5ul.分彆于再灌註2、6、12、24和72 h時,處死6隻大鼠,取腦組織,行HE染色,光鏡下觀察病理學結果,採用免疫組化法測定海馬CA1區caspase-3錶達.分彆于再灌註2、6、12、24和72 h時,處死6隻大鼠,取海馬組織,採用流式細胞儀檢測細胞凋亡率.結果 與S組比較,I/R組和L組再灌註各時點海馬CA1區caspase-3錶達上調,海馬組織細胞凋亡率升高(P<0.01);與I/R組比較,L組再灌註各時點海馬CA1區caspase-3錶達下調,海馬組織細胞凋亡率降低(P<0.01),病理學損傷減輕.結論脂氧素A4後處理減輕大鼠全腦缺血再灌註損傷的機製與下調caspase-3錶達,減少細胞凋亡有關.
목적 평개지양소A4시처리대대서전뇌결혈재관주시세포조망적영향.방법 웅성성년SD대서180지,체중200 ~ 250 g,채용수궤수자표법,장기분위3조:가수술조(S조)、결혈재관주조(I/R조)화지양소A4후처리조(L조).I/R조화L조채용사혈관조새법건립대서전뇌결혈재관주손상모형.L조우재관주즉각측뇌실주사지양소A4 100 ng(용생리염수희석지5ul),S조화I/R조측뇌실주사생리염수5ul.분별우재관주2、6、12、24화72 h시,처사6지대서,취뇌조직,행HE염색,광경하관찰병이학결과,채용면역조화법측정해마CA1구caspase-3표체.분별우재관주2、6、12、24화72 h시,처사6지대서,취해마조직,채용류식세포의검측세포조망솔.결과 여S조비교,I/R조화L조재관주각시점해마CA1구caspase-3표체상조,해마조직세포조망솔승고(P<0.01);여I/R조비교,L조재관주각시점해마CA1구caspase-3표체하조,해마조직세포조망솔강저(P<0.01),병이학손상감경.결론지양소A4후처리감경대서전뇌결혈재관주손상적궤제여하조caspase-3표체,감소세포조망유관.
Objective To evaluate the effect of lipoxin A4 postconditioning on the cell apoptosis following global cerebral ischemia-reperfusion (I/R) in rats.Methods One hundred and eighty healthy male Sprague-Daw-ley rats,weighing 200-250 g,were randomly divided into 3 groups (n =60 each):sham operation group (group S),global cerebral I/R group (group I/R) and lipoxin A4 postconditioning group (group L).Global cerebral I/R was produced by 4-vessel occlusion method in anesthetized rats.Lipoxin A4 100 ng (in 5 μl normal saline) was injected into the lateral cerebral ventricle at the beginning of reperfusion in group L,while the equal volume of normal saline was given instead in groups S and I/R.Six rats were sacrificed at 2,6,12,24 and 72 h of reperfusion and their brains were removed and cut into sections which were stained with haematoxylin and eosin for examination of pathological changes.The expression of caspase-3 in hippocampal CA1 region was detected.Six rats were sacririced at 2,6,12,24 and 72 h of reperfusion and hippocampi were removed for detection of cell apoptosis.The apoptosis rate was calculated.Results Compared with group S,the expression of caspase-3 in hippocampal CA1 region was significantly up-regulated,the apoptosis rate was increased at each time point of reperfusion in groups I/R and L (P < 0.01).Compared with group I/R,the expression of caspase-3 in hippocampal CA1 region was significantly down-regulated,and the apoptosis rate was decreased at each time point of reperfusion (P < 0.01),and the pathological changes were significantly reduced in group L.Conclusion The mechanism by which lipoxin A4 postconditioning ameliorates global cerebral I/R injury is related to down-regulation of caspase-3 expression and reduction of cell apoptosis in rats.