中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2012年
12期
1488-1490
,共3页
汤为香%王立奎%王义桥%杨秀丽%高之心%沈玉君%李元海
湯為香%王立奎%王義橋%楊秀麗%高之心%瀋玉君%李元海
탕위향%왕립규%왕의교%양수려%고지심%침옥군%리원해
二异丙酚%再灌注损伤%脑%内质网%应激%细胞凋亡%预先给药
二異丙酚%再灌註損傷%腦%內質網%應激%細胞凋亡%預先給藥
이이병분%재관주손상%뇌%내질망%응격%세포조망%예선급약
Propofol%Reperfusion injury%Brain%Endoplasmic reticulum%Stress%Apoptosis
目的 评价异丙酚预先给药对大鼠局灶性脑缺血再灌注损伤时内质网应激性细胞凋亡的影响.方法 健康成年雄性SD大鼠80只,体重240~280 g,采用随机数字表法,将大鼠随机分为4组(n=20):假手术组(S组);局灶性脑缺血再灌注组(FCIR组)采用阻塞大脑中动脉4h恢复灌注的方法制备大鼠局灶性脑缺血再灌注模型;异丙酚预先给药组(P组)于缺血前30 min股静脉泵注异丙酚12mg·kg-1·h-1至缺血15min;脂肪乳预先给药组(Ⅰ组)给予脂肪乳1.2 ml·kg-1·h-1.于再灌注6h时各组随机取10只大鼠采用Longa评分法行神经功能缺陷评分(NDS),处死取左侧大脑,用干湿重法测定脑含水量,余10只大鼠处死后取左侧海马,采用Western blot法检测C/EBP环磷酸腺苷反应元件结合转录因子同源蛋白(CHOP)、Bcl-2和活化型caspase-3蛋白的表达水平.结果 与S组比较,FCIR组再灌注6h时NDS评分和脑含水量升高,CHOP和活化型caspase-3蛋白表达上调,Bcl-2蛋白表达下调,P组NDS评分升高(P<0.05);与FCIR组比较,P组再灌注6h时NDS评分和脑含水量降低,CHOP和活化型caspase-3蛋白表达下调,Bcl-2蛋白表达上调(P<0.05),Ⅰ组各指标差异无统计学意义(P>0.05).结论 异丙酚可通过抑制内质网应激介导的细胞凋亡减轻大鼠局灶性脑缺血再灌注损伤.
目的 評價異丙酚預先給藥對大鼠跼竈性腦缺血再灌註損傷時內質網應激性細胞凋亡的影響.方法 健康成年雄性SD大鼠80隻,體重240~280 g,採用隨機數字錶法,將大鼠隨機分為4組(n=20):假手術組(S組);跼竈性腦缺血再灌註組(FCIR組)採用阻塞大腦中動脈4h恢複灌註的方法製備大鼠跼竈性腦缺血再灌註模型;異丙酚預先給藥組(P組)于缺血前30 min股靜脈泵註異丙酚12mg·kg-1·h-1至缺血15min;脂肪乳預先給藥組(Ⅰ組)給予脂肪乳1.2 ml·kg-1·h-1.于再灌註6h時各組隨機取10隻大鼠採用Longa評分法行神經功能缺陷評分(NDS),處死取左側大腦,用榦濕重法測定腦含水量,餘10隻大鼠處死後取左側海馬,採用Western blot法檢測C/EBP環燐痠腺苷反應元件結閤轉錄因子同源蛋白(CHOP)、Bcl-2和活化型caspase-3蛋白的錶達水平.結果 與S組比較,FCIR組再灌註6h時NDS評分和腦含水量升高,CHOP和活化型caspase-3蛋白錶達上調,Bcl-2蛋白錶達下調,P組NDS評分升高(P<0.05);與FCIR組比較,P組再灌註6h時NDS評分和腦含水量降低,CHOP和活化型caspase-3蛋白錶達下調,Bcl-2蛋白錶達上調(P<0.05),Ⅰ組各指標差異無統計學意義(P>0.05).結論 異丙酚可通過抑製內質網應激介導的細胞凋亡減輕大鼠跼竈性腦缺血再灌註損傷.
목적 평개이병분예선급약대대서국조성뇌결혈재관주손상시내질망응격성세포조망적영향.방법 건강성년웅성SD대서80지,체중240~280 g,채용수궤수자표법,장대서수궤분위4조(n=20):가수술조(S조);국조성뇌결혈재관주조(FCIR조)채용조새대뇌중동맥4h회복관주적방법제비대서국조성뇌결혈재관주모형;이병분예선급약조(P조)우결혈전30 min고정맥빙주이병분12mg·kg-1·h-1지결혈15min;지방유예선급약조(Ⅰ조)급여지방유1.2 ml·kg-1·h-1.우재관주6h시각조수궤취10지대서채용Longa평분법행신경공능결함평분(NDS),처사취좌측대뇌,용간습중법측정뇌함수량,여10지대서처사후취좌측해마,채용Western blot법검측C/EBP배린산선감반응원건결합전록인자동원단백(CHOP)、Bcl-2화활화형caspase-3단백적표체수평.결과 여S조비교,FCIR조재관주6h시NDS평분화뇌함수량승고,CHOP화활화형caspase-3단백표체상조,Bcl-2단백표체하조,P조NDS평분승고(P<0.05);여FCIR조비교,P조재관주6h시NDS평분화뇌함수량강저,CHOP화활화형caspase-3단백표체하조,Bcl-2단백표체상조(P<0.05),Ⅰ조각지표차이무통계학의의(P>0.05).결론 이병분가통과억제내질망응격개도적세포조망감경대서국조성뇌결혈재관주손상.
Objective To evaluate the effect of propofol on the endoplasmic reticulum stress-mediated apoptosis during focal cerebral ischemia-reperfusion (I/R) in rats.Methods Eighty adult male Sprague-Dawley rats,weighing 240-280 g,were randomly divided into 4 groups (n =20 each):shame operation group (group S) ; focal cerebral I/R group (group FCIR); propofol pretreatment group (group P); intralipid pretreatment group (group Ⅰ).Focal cerebral I/R was induced by 4 h middle cerebral artery occlusion followed by reperfusion.Propofol was infused at a rate of 12 mg· kg-1 · h-1 starting from 30 min before ischemia until 15 min of ischemia in group P,while intralipid was given instead of propofol in group I.Neurological deficit scores (NDSs) were measured at 6 h of reperfusion in 10 rats chosen from each group and the rats were then sacrificed.Their left brains were removed for determination of brain water content.The left 10 rats were sacrificed and their brains were immediately removed for determination of the expression of C/EBP homologous protein (CHOP),Bcl-2,and activated caspase-3 in the left hippocampi by Western blot.Results Compared with group S,NDSs and brain water content were significantly increased,the expression of CHOP and activated caspase-3 was up-regulated,and the expression of Bcl-2 was down-regulated in group FCIR,NDSs was increased in group P (P < 0.05).Compared with group FCIR,NDSs and brain water content were significantly decreased,the expression of CHOP and activated caspase-3 was down-regulated,and the expression of Bcl-2 was up-regulated in group P,and no significant change was found in each parameter in group Ⅰ (P > 0.05).Conclusion Propofol can reduce focal cerebral I/R injury through inhibition of the endoplasmic reticulum stress-mediated apoptosis in rats.