中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2012年
8期
985-987
,共3页
高操%杨璐%沈江%洪涛%张弦%丁倩%高昌俊%柴伟
高操%楊璐%瀋江%洪濤%張絃%丁倩%高昌俊%柴偉
고조%양로%침강%홍도%장현%정천%고창준%시위
硫化氢%休克,出血性%心肌再灌注损伤%NF-κB
硫化氫%休剋,齣血性%心肌再灌註損傷%NF-κB
류화경%휴극,출혈성%심기재관주손상%NF-κB
Hydrogen sulfide%Shock,hemorrhagic%Myocardial reperfusion injury%NF-kappa B
目的 评价外源性硫化氢对失血性休克复苏大鼠心肌细胞NF-κB活性的影响.方法 清洁级成年雄性SD大鼠40只,体重250 ～ 300 g,采用随机数字表法,将其随机分为4组(n=10)；假手术组(Sham组)、假手术+硫氢化钠组(Sham+ NaHS组)、失血性休克组(HS组)和失血休克+硫氢化钠组(HS+ NaHS组).HS组采用股动脉放血的方法制备大鼠失血性休克模型；HS+ NaHS组失血性休克后复苏前10 min腹腔注射NaHS 28 μmol/kg,Sham+ NaHS组同时点腹腔注射28 μmol/kg NaHS.于放血即刻、放血后1.5、2、3、4和6h时记录大鼠MAP,随后处死大鼠取心脏,采用Western blot法测定心肌细胞pIKKβ、pIκBα、pNF-κB p65和HMGB1表达,光镜和电镜下观察心肌组织超微结构.结果 与Sham组和Sham+ NaHS组相比,HS组和HS+ NaHS组MAP降低,心肌细胞pIKKβ、pIκBα、pNF-κB p65和HMGB1表达上调(P＜ 0.05)；与HS组相比,HS+ NaHS组MAP升高,心肌细胞pIKKβ、pIκBα、pNF-κB p65和HMGB1表达下调(P＜0.05).HS+ NaHS组心肌病理学损伤较HS组减轻.结论 外源性硫化氢可抑制NF-κB活性,减轻炎性反应,从而减轻失血性休克复苏大鼠的心肌损伤.
目的 評價外源性硫化氫對失血性休剋複囌大鼠心肌細胞NF-κB活性的影響.方法 清潔級成年雄性SD大鼠40隻,體重250 ～ 300 g,採用隨機數字錶法,將其隨機分為4組(n=10)；假手術組(Sham組)、假手術+硫氫化鈉組(Sham+ NaHS組)、失血性休剋組(HS組)和失血休剋+硫氫化鈉組(HS+ NaHS組).HS組採用股動脈放血的方法製備大鼠失血性休剋模型；HS+ NaHS組失血性休剋後複囌前10 min腹腔註射NaHS 28 μmol/kg,Sham+ NaHS組同時點腹腔註射28 μmol/kg NaHS.于放血即刻、放血後1.5、2、3、4和6h時記錄大鼠MAP,隨後處死大鼠取心髒,採用Western blot法測定心肌細胞pIKKβ、pIκBα、pNF-κB p65和HMGB1錶達,光鏡和電鏡下觀察心肌組織超微結構.結果 與Sham組和Sham+ NaHS組相比,HS組和HS+ NaHS組MAP降低,心肌細胞pIKKβ、pIκBα、pNF-κB p65和HMGB1錶達上調(P＜ 0.05)；與HS組相比,HS+ NaHS組MAP升高,心肌細胞pIKKβ、pIκBα、pNF-κB p65和HMGB1錶達下調(P＜0.05).HS+ NaHS組心肌病理學損傷較HS組減輕.結論 外源性硫化氫可抑製NF-κB活性,減輕炎性反應,從而減輕失血性休剋複囌大鼠的心肌損傷.
목적 평개외원성류화경대실혈성휴극복소대서심기세포NF-κB활성적영향.방법 청길급성년웅성SD대서40지,체중250 ～ 300 g,채용수궤수자표법,장기수궤분위4조(n=10)；가수술조(Sham조)、가수술+류경화납조(Sham+ NaHS조)、실혈성휴극조(HS조)화실혈휴극+류경화납조(HS+ NaHS조).HS조채용고동맥방혈적방법제비대서실혈성휴극모형；HS+ NaHS조실혈성휴극후복소전10 min복강주사NaHS 28 μmol/kg,Sham+ NaHS조동시점복강주사28 μmol/kg NaHS.우방혈즉각、방혈후1.5、2、3、4화6h시기록대서MAP,수후처사대서취심장,채용Western blot법측정심기세포pIKKβ、pIκBα、pNF-κB p65화HMGB1표체,광경화전경하관찰심기조직초미결구.결과 여Sham조화Sham+ NaHS조상비,HS조화HS+ NaHS조MAP강저,심기세포pIKKβ、pIκBα、pNF-κB p65화HMGB1표체상조(P＜ 0.05)；여HS조상비,HS+ NaHS조MAP승고,심기세포pIKKβ、pIκBα、pNF-κB p65화HMGB1표체하조(P＜0.05).HS+ NaHS조심기병이학손상교HS조감경.결론 외원성류화경가억제NF-κB활성,감경염성반응,종이감경실혈성휴극복소대서적심기손상.
Objective To investigate the effect of exogenous hydrogen sulfide on myocardial NF-κB signaling pathway in rats with hemorrhagic shock (HS).Methods Forty adult male rats,weighing 250-300 g,were randomly divided into 4 groups (n =10 each):sham operation group (Sham group),sham operation + NaHS group (Sham + NaHS group),HS group and HS + NaHS group.HS was induced by withdrawing blood from the femoral artery.After HS,NaHS 28 μmol/kg was injected intraperitoneally at 10 min before resuscitation in groups HS + NaHS and Sham + NaHS.MAP was monitored and recorded at 0,1.5,2,3,4 and 6 h after blood-letting.The rats were then sacrificed and hearts were removed for determination of phosphorylated IKKβ (pIKKβ),IκBα (pIκBα),NF-κB p65 (pNF-κB p65) and high-mobility group box 1 (HMGB1) and for examination of myocardial ultrastructure with light and electron microscope.Results Compared with Sham and Sham + NaSH groups,MAP was significantly decreased and the expression of pIKKβ,pIκBα,pNF-κB p65 and HMGB1 was up-regulated in HS and HS + NaHS groups (P ＜ 0.05).Compared with HS group,MAP was significantly increased and the expression of pIKKβ,pIκBα,pNF-κB p65 and HMGB1 was down-regulated in HS + NaHS group (P ＜ 0.05).The pathologic changes were attenuated in HS + NaHS group compared with group HS.Conclusion Exogenous hydrogen sulfide can attenuate myocardial injury induced by HS through inhibition of NF-κB signaling pathway and reduction of inflammatory response.
