中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2011年
9期
1110-1113
,共4页
李新%罗鹏%王枫%王世全%李艳%杨谦梓%李旭颖%王强%熊利泽
李新%囉鵬%王楓%王世全%李豔%楊謙梓%李旭穎%王彊%熊利澤
리신%라붕%왕풍%왕세전%리염%양겸재%리욱영%왕강%웅리택
肿瘤抑制蛋白质类%麻醉药,吸入%缺血预处理%再灌注损伤%脑
腫瘤抑製蛋白質類%痳醉藥,吸入%缺血預處理%再灌註損傷%腦
종류억제단백질류%마취약,흡입%결혈예처리%재관주손상%뇌
Tumor suppressor proteins%Anesthetics,inhalation%Ischemic preconditioning%Reperfusion injury%Brain
目的 评价N-myc下游调节基因2(NDRG2)在七氟醚预处理减轻大鼠局灶性脑缺血再灌注损伤中的作用.方法 健康雄性成年SD大鼠48只,体重280~320 g,采用随机数字表,将大鼠随机分为3组(n=16):假手术组(S组)、脑缺血再灌注组(I/R组)和七氟醚预处理组(Sev组).采用大脑中动脉阻断法制备大鼠局灶性脑缺血再灌注模型.大鼠吸入2%七氟醚lh,每天1次,连续5d行七氟醚预处理.Sev组于七氟醚预处理结束后24h制备局灶性脑缺血再灌注模型.再灌注24h时行神经功能评分,随后处死大鼠,取脑组织,测定脑梗死体积百分比,采用Western Blot法测定缺血半暗带区NDRG2和活化的Caspase-3的表达,采用免疫组织荧光测定缺血半暗带区NDRG2的表达及定位.结果 与S组比较,I/R组和Sev组脑梗死体积百分比升高,神经功能评分降低,脑组织缺血区半暗带NDRG2和活化的Caspase-3表达上调(P<0.05);与I/R组比较,Sev组脑梗死体积百分比降低,神经功能评分升高,脑组织缺血区半暗带NDRG2和活化的Caspase-3表达下调(P<0.05).Sev组核内NDRG2阳性染色较I/R组减浅.结论 七氟醚预处理可能通过抑制脑组织NDRG2的表达、活性和细胞凋亡,从而减轻大鼠局灶性脑缺血再灌注损伤.
目的 評價N-myc下遊調節基因2(NDRG2)在七氟醚預處理減輕大鼠跼竈性腦缺血再灌註損傷中的作用.方法 健康雄性成年SD大鼠48隻,體重280~320 g,採用隨機數字錶,將大鼠隨機分為3組(n=16):假手術組(S組)、腦缺血再灌註組(I/R組)和七氟醚預處理組(Sev組).採用大腦中動脈阻斷法製備大鼠跼竈性腦缺血再灌註模型.大鼠吸入2%七氟醚lh,每天1次,連續5d行七氟醚預處理.Sev組于七氟醚預處理結束後24h製備跼竈性腦缺血再灌註模型.再灌註24h時行神經功能評分,隨後處死大鼠,取腦組織,測定腦梗死體積百分比,採用Western Blot法測定缺血半暗帶區NDRG2和活化的Caspase-3的錶達,採用免疫組織熒光測定缺血半暗帶區NDRG2的錶達及定位.結果 與S組比較,I/R組和Sev組腦梗死體積百分比升高,神經功能評分降低,腦組織缺血區半暗帶NDRG2和活化的Caspase-3錶達上調(P<0.05);與I/R組比較,Sev組腦梗死體積百分比降低,神經功能評分升高,腦組織缺血區半暗帶NDRG2和活化的Caspase-3錶達下調(P<0.05).Sev組覈內NDRG2暘性染色較I/R組減淺.結論 七氟醚預處理可能通過抑製腦組織NDRG2的錶達、活性和細胞凋亡,從而減輕大鼠跼竈性腦缺血再灌註損傷.
목적 평개N-myc하유조절기인2(NDRG2)재칠불미예처리감경대서국조성뇌결혈재관주손상중적작용.방법 건강웅성성년SD대서48지,체중280~320 g,채용수궤수자표,장대서수궤분위3조(n=16):가수술조(S조)、뇌결혈재관주조(I/R조)화칠불미예처리조(Sev조).채용대뇌중동맥조단법제비대서국조성뇌결혈재관주모형.대서흡입2%칠불미lh,매천1차,련속5d행칠불미예처리.Sev조우칠불미예처리결속후24h제비국조성뇌결혈재관주모형.재관주24h시행신경공능평분,수후처사대서,취뇌조직,측정뇌경사체적백분비,채용Western Blot법측정결혈반암대구NDRG2화활화적Caspase-3적표체,채용면역조직형광측정결혈반암대구NDRG2적표체급정위.결과 여S조비교,I/R조화Sev조뇌경사체적백분비승고,신경공능평분강저,뇌조직결혈구반암대NDRG2화활화적Caspase-3표체상조(P<0.05);여I/R조비교,Sev조뇌경사체적백분비강저,신경공능평분승고,뇌조직결혈구반암대NDRG2화활화적Caspase-3표체하조(P<0.05).Sev조핵내NDRG2양성염색교I/R조감천.결론 칠불미예처리가능통과억제뇌조직NDRG2적표체、활성화세포조망,종이감경대서국조성뇌결혈재관주손상.
Objective To investigate the role of N-myc downstream regulated genes 2 (NDRG2) in attenuation of focal cerebral ischemic-reperfusin injury by sevoflurane preconditioning in rats.Methods Forty-eight healthy male SD rats weighing 280-320 g were randomly divided into 3 groups ( n =16 each):sham operation group (group S),ischemia-reperfusion injury group (group I/R) and sevoflurane preconditioning group (group Sev).Focal cerebral ischemia-reperfusion injury was induced by right middle cerebral artery occlusion (MCAO)for 120 min followed by 24 h reperfusion.In group Sev,2.0% sevoflurane was inhaled 1 h once a day for 5 consecutive days at 24 h before MCAO.The neurologic function was evaluated at 24 h of reperfusion and than the rats were sacrificed,and the brain was removed for determination of infarct volume percentage,NDRG2 and activated Caspase-3 expression in ischemic penumbra by Western Blot and NDRG2 expression and location by immunohistochemistry.Results The infarct volume percentage,NDRG2 and activated Caspase-3 expression were higher,and neurologic function score was lower in groups I/R and Sev then in group S( P < 0.05).The infarct volume percentage,NDRG2 and activated Caspase-3 expression were lower,and neurologic function score was higher in group Sev then in group I/R ( P < 0.05).The intranuclear NDRG2 positive staining was decreased in group Sev than in group I/R.Conclusion Sevoflurane preconditioning can reduce focal cerebral ischemia-reperfusion injury by inhibiting the expression and activity of NDRG2 and apoptosis in rats.