国际麻醉学与复苏杂志
國際痳醉學與複囌雜誌
국제마취학여복소잡지
INTERNATIONAL JOURNAL OF ANESTHESIOLOGY AND RESUSCITATION
2010年
5期
394-397,420
,共5页
王艳婷%王士雷%常庆显%李瑜%江岩%王世端
王豔婷%王士雷%常慶顯%李瑜%江巖%王世耑
왕염정%왕사뢰%상경현%리유%강암%왕세단
缺血/再灌注损伤%克罗卡林%水通道蛋白-4%血脑屏障
缺血/再灌註損傷%剋囉卡林%水通道蛋白-4%血腦屏障
결혈/재관주손상%극라잡림%수통도단백-4%혈뇌병장
Ischemia-reperfusion injury%Cromakalim%AQP-4%Blood brain barrier
目的 研究ATP敏感性钾通道(KATP)开放剂克罗卡林对大鼠脑缺血/再灌注(ischemia/reperfusion,I/R)后水通道蛋白4(aquaporin-4,AQP-4)表达及血脑屏障(blood-brain-barrier,BBB)通透性的影响. 方法 30只健康雄性Wistar大鼠参照随机数目表按三组安全随机分组法分为假手术组(A组)、脑I/R对照组(B组)、脑I/R+克罗卡林组(C组),每组10只.应用线栓法建立大鼠大脑中动脉缺血(middle cerebral artery occlusion,MCAO)模型,脑缺血2 h再灌注24h后,观察动物神经行为缺损,并取脑检查.Bederson法评价动物的神经行为功能,应用苏木素-伊红(HE)染色观察病理变化,干湿重法测定脑组织含水量,并通过免疫组织化学方法检测IgG及AQP-4的表达. 结果 与A组脑含水量(78.2±1.3)%,IgG、AQP-4蛋白表达(0.0±0.0,13.6±1.5)相比,B组脑含水量(81.3±1.2)%,IgG、AQP-4蛋白表达(2.4±0.4,19.8±1.9)均明显增高(P<0.05),而C组脑含水量(79.5±0.6)%变化则差异无统计学意义(P>0.05),但IgG与AQP-4的表达(1.1±0.2,15.7±1.2)也明显升高(P<0.05);与B组相比,C组神经行为缺损评分明显减低(P<0.05),IgG、AQP-4(1.1±0.2,15.7±1.2)蛋白表达及脑组织含水量(79.5±0.6)%亦明显降低(P<0.05).结论 脑I/R损伤过程中,克罗卡林可能通过降低AQP-4的表达和BBB的通透性,减轻脑水肿,发挥脑保护作用.
目的 研究ATP敏感性鉀通道(KATP)開放劑剋囉卡林對大鼠腦缺血/再灌註(ischemia/reperfusion,I/R)後水通道蛋白4(aquaporin-4,AQP-4)錶達及血腦屏障(blood-brain-barrier,BBB)通透性的影響. 方法 30隻健康雄性Wistar大鼠參照隨機數目錶按三組安全隨機分組法分為假手術組(A組)、腦I/R對照組(B組)、腦I/R+剋囉卡林組(C組),每組10隻.應用線栓法建立大鼠大腦中動脈缺血(middle cerebral artery occlusion,MCAO)模型,腦缺血2 h再灌註24h後,觀察動物神經行為缺損,併取腦檢查.Bederson法評價動物的神經行為功能,應用囌木素-伊紅(HE)染色觀察病理變化,榦濕重法測定腦組織含水量,併通過免疫組織化學方法檢測IgG及AQP-4的錶達. 結果 與A組腦含水量(78.2±1.3)%,IgG、AQP-4蛋白錶達(0.0±0.0,13.6±1.5)相比,B組腦含水量(81.3±1.2)%,IgG、AQP-4蛋白錶達(2.4±0.4,19.8±1.9)均明顯增高(P<0.05),而C組腦含水量(79.5±0.6)%變化則差異無統計學意義(P>0.05),但IgG與AQP-4的錶達(1.1±0.2,15.7±1.2)也明顯升高(P<0.05);與B組相比,C組神經行為缺損評分明顯減低(P<0.05),IgG、AQP-4(1.1±0.2,15.7±1.2)蛋白錶達及腦組織含水量(79.5±0.6)%亦明顯降低(P<0.05).結論 腦I/R損傷過程中,剋囉卡林可能通過降低AQP-4的錶達和BBB的通透性,減輕腦水腫,髮揮腦保護作用.
목적 연구ATP민감성갑통도(KATP)개방제극라잡림대대서뇌결혈/재관주(ischemia/reperfusion,I/R)후수통도단백4(aquaporin-4,AQP-4)표체급혈뇌병장(blood-brain-barrier,BBB)통투성적영향. 방법 30지건강웅성Wistar대서삼조수궤수목표안삼조안전수궤분조법분위가수술조(A조)、뇌I/R대조조(B조)、뇌I/R+극라잡림조(C조),매조10지.응용선전법건립대서대뇌중동맥결혈(middle cerebral artery occlusion,MCAO)모형,뇌결혈2 h재관주24h후,관찰동물신경행위결손,병취뇌검사.Bederson법평개동물적신경행위공능,응용소목소-이홍(HE)염색관찰병리변화,간습중법측정뇌조직함수량,병통과면역조직화학방법검측IgG급AQP-4적표체. 결과 여A조뇌함수량(78.2±1.3)%,IgG、AQP-4단백표체(0.0±0.0,13.6±1.5)상비,B조뇌함수량(81.3±1.2)%,IgG、AQP-4단백표체(2.4±0.4,19.8±1.9)균명현증고(P<0.05),이C조뇌함수량(79.5±0.6)%변화칙차이무통계학의의(P>0.05),단IgG여AQP-4적표체(1.1±0.2,15.7±1.2)야명현승고(P<0.05);여B조상비,C조신경행위결손평분명현감저(P<0.05),IgG、AQP-4(1.1±0.2,15.7±1.2)단백표체급뇌조직함수량(79.5±0.6)%역명현강저(P<0.05).결론 뇌I/R손상과정중,극라잡림가능통과강저AQP-4적표체화BBB적통투성,감경뇌수종,발휘뇌보호작용.
Objective To investigate the effects of ATP-sensitive potassium channel openers (Cromakalim) on the expression of aquaporin-4 and permeability of blood-brain barrer (BBB) after cerebral ischemic/repeffusion. Methods Thirty healthy male Wistar rats were randomized into three groups for different conditioning, the sham-operated group(A,n=10), the cerebral I/R group(B,n=10),and the cerebral I/R+Cromakalim group (C,n=10). Intraluminal suture methods were applied to establish the middle cerebral artery occlusion(MCAO) model with occlusion 2 h and reperfusion 24 h. The neurobehavioral function was evaluated with Bederson's test, and the pathological changes were observed with hematoxylin-eosin(HE) staining. The water content of brain was evaluated by wet-dry weight method, and the expressions of IgG and AQP-4 in brain were observed by immunohistochemistry staining. Results In comparison with group A's water content(78.2±1.3 )% and expressions of IgG and AQP-4 (0.0±0.0,13.6±1.5) ,the expressions of IgG and AQP-4(2.4±0.4,19.8±1.9) and the water content (81.3±1.2)% in group B both were significantly higher (P<0.05). However,in group C,the water content (79.5±0.6)%was similar to group A( 78.2± 1.3 )%. Interestingly, the expressions of IgG and AQP-4( 1.1 ±0.2, 15.7± 1.2 ) of group C were higher than that of group A' s (P<0.05); compared with group B, The neurobehavioral deficit scores were obviously reduced, the expressions of IgG and AQP-4 (1.1 ±0.2,15.7±1.2) and the water content (79.5 ±0.6)% were significantly lower in group C (P<0.05).Conclusion Cromakalim maybe can alleviate cerebral edema via reducing permeability of blood-brain barrier and inhibit the expression of AQP-4 in cerebral ischemia/reperfusion mice.