中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2015年
3期
307-309
,共3页
右美托咪啶%再灌注损伤%脑%JNK丝裂原活化蛋白激酶类
右美託咪啶%再灌註損傷%腦%JNK絲裂原活化蛋白激酶類
우미탁미정%재관주손상%뇌%JNK사렬원활화단백격매류
Dexmedetomidine%Reperfusion injury%Brain%JNK mitogen-activated protein kinases
目的 评价右美托咪定对大鼠脑缺血再灌注时c-Jun氨基末端激酶(JNK)活性的影响.方法 清洁级健康雄性SD大鼠81只,8周龄,体重180 ～ 220 g,采用随机数字法分为3组(n=27):假手术组(S组)、脑缺血再灌注组(CI/R组)和右美托咪定组(Dex组).CI/R组和Dex组采用线栓法制备大鼠脑缺血再灌注损伤模型,缺血2h,再灌注24 h,S组仅分离动脉不置入线栓;Dex组于缺血前即刻尾静脉注射右美托咪定3 μg/kg,随后以3μg·kg-1·h-1速率输注至再灌注24 h,S组和CI/R组给予等容量生理盐水.于再灌注24 h时处死大鼠取脑组织,采用TTC法测定脑梗死体积,计算脑梗死体积百分比;采用干湿法测定脑含水量;采用TUNEL法染色,计数凋亡细胞,计算细胞凋亡指数,采用Western blot法检测磷酸化c-Jun氨基末端激酶(p-JNK)的表达水平.结果 与S组比较,CI/R组和Dex组脑含水量、细胞凋亡指数和脑梗死体积百分比升高,p-JNK表达上调(P＜0.05);与CI/R组比较,Dex组脑含水量、细胞凋亡指数和脑梗死体积百分比降低,p-JNK表达F调(P＜0.05).结论 右美托咪定通过降低JNK活性抑制细胞凋亡减轻大鼠脑缺血再灌注损伤.
目的 評價右美託咪定對大鼠腦缺血再灌註時c-Jun氨基末耑激酶(JNK)活性的影響.方法 清潔級健康雄性SD大鼠81隻,8週齡,體重180 ～ 220 g,採用隨機數字法分為3組(n=27):假手術組(S組)、腦缺血再灌註組(CI/R組)和右美託咪定組(Dex組).CI/R組和Dex組採用線栓法製備大鼠腦缺血再灌註損傷模型,缺血2h,再灌註24 h,S組僅分離動脈不置入線栓;Dex組于缺血前即刻尾靜脈註射右美託咪定3 μg/kg,隨後以3μg·kg-1·h-1速率輸註至再灌註24 h,S組和CI/R組給予等容量生理鹽水.于再灌註24 h時處死大鼠取腦組織,採用TTC法測定腦梗死體積,計算腦梗死體積百分比;採用榦濕法測定腦含水量;採用TUNEL法染色,計數凋亡細胞,計算細胞凋亡指數,採用Western blot法檢測燐痠化c-Jun氨基末耑激酶(p-JNK)的錶達水平.結果 與S組比較,CI/R組和Dex組腦含水量、細胞凋亡指數和腦梗死體積百分比升高,p-JNK錶達上調(P＜0.05);與CI/R組比較,Dex組腦含水量、細胞凋亡指數和腦梗死體積百分比降低,p-JNK錶達F調(P＜0.05).結論 右美託咪定通過降低JNK活性抑製細胞凋亡減輕大鼠腦缺血再灌註損傷.
목적 평개우미탁미정대대서뇌결혈재관주시c-Jun안기말단격매(JNK)활성적영향.방법 청길급건강웅성SD대서81지,8주령,체중180 ～ 220 g,채용수궤수자법분위3조(n=27):가수술조(S조)、뇌결혈재관주조(CI/R조)화우미탁미정조(Dex조).CI/R조화Dex조채용선전법제비대서뇌결혈재관주손상모형,결혈2h,재관주24 h,S조부분리동맥불치입선전;Dex조우결혈전즉각미정맥주사우미탁미정3 μg/kg,수후이3μg·kg-1·h-1속솔수주지재관주24 h,S조화CI/R조급여등용량생리염수.우재관주24 h시처사대서취뇌조직,채용TTC법측정뇌경사체적,계산뇌경사체적백분비;채용간습법측정뇌함수량;채용TUNEL법염색,계수조망세포,계산세포조망지수,채용Western blot법검측린산화c-Jun안기말단격매(p-JNK)적표체수평.결과 여S조비교,CI/R조화Dex조뇌함수량、세포조망지수화뇌경사체적백분비승고,p-JNK표체상조(P＜0.05);여CI/R조비교,Dex조뇌함수량、세포조망지수화뇌경사체적백분비강저,p-JNK표체F조(P＜0.05).결론 우미탁미정통과강저JNK활성억제세포조망감경대서뇌결혈재관주손상.
Objective To evaluate the effects of dexmedetomidine on the activity of c-Jun N-terminal kinase (JNK) during cerebral ischemia-reperfusion (I/R) in rats.Methods Eighty-one pathogen-free male Sprague-Dawley rats,aged 8 weeks,weighing 180-220 g,were randomly divided into 3 groups (n=27 each) using a random number table:sham operation group (group S);cerebral I/R group (group CI/R);dexmedetomidine group (group Dex).The rats were anesthetized with intraperitoneal 10％ chloral hydrate 300 mg/kg.Cerebral ischemia was induced by occlusion of the middle cerebral artery for 2 h followed by 24 h of reperfusion in CI/R and Dex groups.The middle cerebral artery was only exposed but not occluded in group S.Dexmedetomidine 3 μg/kg was injected via the tail vein immediately before ischemia followed by infusion at a rate of 3 μg · kg-1 · h-1until 24 h of reperfusion in group Dex,while the equal volume of normal saline was given in S and CI/R groups.The rats were sacrificed at 24 h of reperfusion,and their brains were removed for determination of cerebral infarct size (by TTC staining),brain water content ((wet weight-dry weight)/wet weight × 100％),cell apoptosis (by TUNEL) and expression of phosphorylated JNK (p-JNK) protein (by Western blot analysis).Apoptotic index was calculated.Results Compared with group S,the brain water content,apoptotic index and cerebral infarct size were significantly increased,and the expression of p-JNK was up-regulated in CI/R and Dex groups.Compared with group CI/R,the brain water content,apoptotic index and cerebral infarct size were significantly decreased,and the expression of p-JNK was down-regulated in group Dex.Conclusion Dexmedetomidine reduces cerebral I/R injury through decreasing the activity of JNK and inhibiting cell apoptosis in rats.
