中华神经医学杂志
中華神經醫學雜誌
중화신경의학잡지
CHINESE JOURNAL OF NEUROMEDICINE
2012年
2期
138-140
,共3页
秦华平%杨常春%张一%谢陶吟%王强%支枫%江基尧
秦華平%楊常春%張一%謝陶吟%王彊%支楓%江基堯
진화평%양상춘%장일%사도음%왕강%지풍%강기요
深低温%脑缺血%细胞色素C%细胞凋亡
深低溫%腦缺血%細胞色素C%細胞凋亡
심저온%뇌결혈%세포색소C%세포조망
Profound hypothermia%Cerebral ischemia%Cytochrome C%Cell apoptosis
目的 观察深低温对全脑缺血大鼠海马线粒体细胞色素C(Cyt-C)释放和细胞凋亡的影响,探讨深低温的脑保护作用机制. 方法 24只SD大鼠建立大鼠体外循环模型后按随机数字表法分成3组:对照组(建立大鼠体外循环模型5 min后迅速处死取海马组织)、常温缺血组[大鼠于(37±0.3)℃下停循环5 min后迅速处死取海马组织)和低温缺血组(热交换器配合体外冰屑诱导使大鼠肛温降至(18±0.5)℃,停循环5 min后迅速处死取海马组织),每组各8只.Western blotting检测3组大鼠海马神经细胞胞浆Cyt-C的表达,TUNEL法检测3组大鼠海马神经细胞凋亡率. 结果 常温缺血组海马神经细胞胞浆Cyt-C浓度(3.57±0.82)较对照组(0.48±0.14)明显升高,而低温缺血组Cyt-C浓度(1.24±0.53)较常温缺血组明显降低,差异均有统计学意义(P<0.05).常温缺血组海马神经细胞凋亡率(50.45%±3.71%)较对照组(2.56%±0.43%)明显升高,而低温缺血组海马神经细胞凋亡率(16.51%±2.65%)较常温缺血组明显降低,差异均有统计学意义(P<0.05). 结论 深低温可抑制全脑缺血大鼠海马线粒体Cyt-C释放和细胞凋亡,是其脑保护作用的重要机制之一.
目的 觀察深低溫對全腦缺血大鼠海馬線粒體細胞色素C(Cyt-C)釋放和細胞凋亡的影響,探討深低溫的腦保護作用機製. 方法 24隻SD大鼠建立大鼠體外循環模型後按隨機數字錶法分成3組:對照組(建立大鼠體外循環模型5 min後迅速處死取海馬組織)、常溫缺血組[大鼠于(37±0.3)℃下停循環5 min後迅速處死取海馬組織)和低溫缺血組(熱交換器配閤體外冰屑誘導使大鼠肛溫降至(18±0.5)℃,停循環5 min後迅速處死取海馬組織),每組各8隻.Western blotting檢測3組大鼠海馬神經細胞胞漿Cyt-C的錶達,TUNEL法檢測3組大鼠海馬神經細胞凋亡率. 結果 常溫缺血組海馬神經細胞胞漿Cyt-C濃度(3.57±0.82)較對照組(0.48±0.14)明顯升高,而低溫缺血組Cyt-C濃度(1.24±0.53)較常溫缺血組明顯降低,差異均有統計學意義(P<0.05).常溫缺血組海馬神經細胞凋亡率(50.45%±3.71%)較對照組(2.56%±0.43%)明顯升高,而低溫缺血組海馬神經細胞凋亡率(16.51%±2.65%)較常溫缺血組明顯降低,差異均有統計學意義(P<0.05). 結論 深低溫可抑製全腦缺血大鼠海馬線粒體Cyt-C釋放和細胞凋亡,是其腦保護作用的重要機製之一.
목적 관찰심저온대전뇌결혈대서해마선립체세포색소C(Cyt-C)석방화세포조망적영향,탐토심저온적뇌보호작용궤제. 방법 24지SD대서건립대서체외순배모형후안수궤수자표법분성3조:대조조(건립대서체외순배모형5 min후신속처사취해마조직)、상온결혈조[대서우(37±0.3)℃하정순배5 min후신속처사취해마조직)화저온결혈조(열교환기배합체외빙설유도사대서항온강지(18±0.5)℃,정순배5 min후신속처사취해마조직),매조각8지.Western blotting검측3조대서해마신경세포포장Cyt-C적표체,TUNEL법검측3조대서해마신경세포조망솔. 결과 상온결혈조해마신경세포포장Cyt-C농도(3.57±0.82)교대조조(0.48±0.14)명현승고,이저온결혈조Cyt-C농도(1.24±0.53)교상온결혈조명현강저,차이균유통계학의의(P<0.05).상온결혈조해마신경세포조망솔(50.45%±3.71%)교대조조(2.56%±0.43%)명현승고,이저온결혈조해마신경세포조망솔(16.51%±2.65%)교상온결혈조명현강저,차이균유통계학의의(P<0.05). 결론 심저온가억제전뇌결혈대서해마선립체Cyt-C석방화세포조망,시기뇌보호작용적중요궤제지일.
Objective To detect the effect and role of profound hypothermia on cytochrome C release and cell apoptosis in the hippocampus after global ischemia in rats. Methods We established the animal model of cardiopulmonary bypass (CPB) in 24 rats which were randomized into 3 even groups:blank control group,normothermia ischemia group and hypothermia ischemia group.After the hippocampus samples were harvested from the 3 groups,Western blot was used to detect the expression of cytochrome C (Cyt-C) and TUNEL was used to measure the cell apoptosis. Results The expression of Cyt-C in the normothermia ischemia group increased significantly compared with the blank control group but decreased significantly compared with the hypothermia ischemia group (P<0.05).The rate of cell apoptosis in the normothermia ischemia group increased significantly compared with the blank control group but decreased significantly compared with the hypothermia ischemia group (P<0.05).Conclusions Profound hypothermia can inhibit cytochrome C release into the cytoplasm and thus reduce cell apoptosis in the hippocampus after global ischemia in rats. This may be one important mechanism underlying the protective effect of profound hypothermia.