中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2014年
10期
1259-1262
,共4页
张萌%李国风%骆海坤%张建新
張萌%李國風%駱海坤%張建新
장맹%리국풍%락해곤%장건신
硫化氢%脑缺血%线粒体
硫化氫%腦缺血%線粒體
류화경%뇌결혈%선립체
Hydrogen sulfide%Brain ischemia%Mitochondria
目的 评价外源性硫化氢(H2S)对大鼠局灶性脑缺血时线粒体功能的影响.方法 健康雄性SD大鼠80只,体重250～300 g,采用随机数字表法分为5组(n=16):假手术组(S组)、脑缺血组(CI组)和NaHS高、中、低剂量组(NaHS1组、NaHS2组和NaHS3组).采用大脑中动脉栓塞法建立大鼠局灶性脑缺血模型.于模型制备后3h,S组和CI组腹腔注射1ml/kg生理盐水.NaHS1组、NaHS2组和NaHS3组分别腹腔注射NaHS 2.8、1.4和0.7 mg/kg.于模型制备后24h时测定脑缺血体积,取缺血侧脑组织,测定H2S含量、3-巯基丙酮酸转硫酶(3MST)活性,并提取脑组织线粒体,测定线粒体活性、线粒体膜肿胀度、线粒体总ATP酶、超氧化物岐化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)活性和丙二醛(MDA)含量.结果 与S组比较,CI组、NaHS1组、NaHS2组和NaHS3组脑缺血体积增大,CI组、NaHS2组和NaHS3组脑组织H2S含量和线粒体3MST活性降低,CI组和NaHS3组线粒体活性、SOD活性和GSH-Px活性降低,线粒体膜肿胀度增加,MDA含量升高,CI组总ATP酶活性降低,NaHS1组和NaHS2组SOD活性降低(P＜0.05);与CI组比较,NaHS1组和NaHS2组脑缺血体积减小,脑组织H2S含量和线粒体3MST活性升高,线粒体活性、总ATP酶活性、SOD活性和GSH-Px活性升高,线粒体膜肿胀度减轻,MDA含量降低(P＜0.05);与NaHS1组比较,NaHS3组线粒体3MST活性降低,线粒体膜肿胀度增加,SOD活性和GSH-Px活性降低(P＜0.05).结论 外源性H2S减轻大鼠局灶性脑缺血损伤的机制与提高线粒体抗氧化能力,减轻线粒体损伤有关.
目的 評價外源性硫化氫(H2S)對大鼠跼竈性腦缺血時線粒體功能的影響.方法 健康雄性SD大鼠80隻,體重250～300 g,採用隨機數字錶法分為5組(n=16):假手術組(S組)、腦缺血組(CI組)和NaHS高、中、低劑量組(NaHS1組、NaHS2組和NaHS3組).採用大腦中動脈栓塞法建立大鼠跼竈性腦缺血模型.于模型製備後3h,S組和CI組腹腔註射1ml/kg生理鹽水.NaHS1組、NaHS2組和NaHS3組分彆腹腔註射NaHS 2.8、1.4和0.7 mg/kg.于模型製備後24h時測定腦缺血體積,取缺血側腦組織,測定H2S含量、3-巰基丙酮痠轉硫酶(3MST)活性,併提取腦組織線粒體,測定線粒體活性、線粒體膜腫脹度、線粒體總ATP酶、超氧化物岐化酶(SOD)、穀胱甘肽過氧化物酶(GSH-Px)活性和丙二醛(MDA)含量.結果 與S組比較,CI組、NaHS1組、NaHS2組和NaHS3組腦缺血體積增大,CI組、NaHS2組和NaHS3組腦組織H2S含量和線粒體3MST活性降低,CI組和NaHS3組線粒體活性、SOD活性和GSH-Px活性降低,線粒體膜腫脹度增加,MDA含量升高,CI組總ATP酶活性降低,NaHS1組和NaHS2組SOD活性降低(P＜0.05);與CI組比較,NaHS1組和NaHS2組腦缺血體積減小,腦組織H2S含量和線粒體3MST活性升高,線粒體活性、總ATP酶活性、SOD活性和GSH-Px活性升高,線粒體膜腫脹度減輕,MDA含量降低(P＜0.05);與NaHS1組比較,NaHS3組線粒體3MST活性降低,線粒體膜腫脹度增加,SOD活性和GSH-Px活性降低(P＜0.05).結論 外源性H2S減輕大鼠跼竈性腦缺血損傷的機製與提高線粒體抗氧化能力,減輕線粒體損傷有關.
목적 평개외원성류화경(H2S)대대서국조성뇌결혈시선립체공능적영향.방법 건강웅성SD대서80지,체중250～300 g,채용수궤수자표법분위5조(n=16):가수술조(S조)、뇌결혈조(CI조)화NaHS고、중、저제량조(NaHS1조、NaHS2조화NaHS3조).채용대뇌중동맥전새법건립대서국조성뇌결혈모형.우모형제비후3h,S조화CI조복강주사1ml/kg생리염수.NaHS1조、NaHS2조화NaHS3조분별복강주사NaHS 2.8、1.4화0.7 mg/kg.우모형제비후24h시측정뇌결혈체적,취결혈측뇌조직,측정H2S함량、3-구기병동산전류매(3MST)활성,병제취뇌조직선립체,측정선립체활성、선립체막종창도、선립체총ATP매、초양화물기화매(SOD)、곡광감태과양화물매(GSH-Px)활성화병이철(MDA)함량.결과 여S조비교,CI조、NaHS1조、NaHS2조화NaHS3조뇌결혈체적증대,CI조、NaHS2조화NaHS3조뇌조직H2S함량화선립체3MST활성강저,CI조화NaHS3조선립체활성、SOD활성화GSH-Px활성강저,선립체막종창도증가,MDA함량승고,CI조총ATP매활성강저,NaHS1조화NaHS2조SOD활성강저(P＜0.05);여CI조비교,NaHS1조화NaHS2조뇌결혈체적감소,뇌조직H2S함량화선립체3MST활성승고,선립체활성、총ATP매활성、SOD활성화GSH-Px활성승고,선립체막종창도감경,MDA함량강저(P＜0.05);여NaHS1조비교,NaHS3조선립체3MST활성강저,선립체막종창도증가,SOD활성화GSH-Px활성강저(P＜0.05).결론 외원성H2S감경대서국조성뇌결혈손상적궤제여제고선립체항양화능력,감경선립체손상유관.
Objective To investigate the effects of exogenous hydrogen sulfide (H2S) on the mitochondrial function during focal cerebral ischemia and the relationship with mitochondrial damage in rats.Methods Eighty male Sprague-Dawley rats,weighing 250-300 g,were randomly divided into 5 groups (n =16 each):sham operation group (group S),cerebral ischemia group (group CI),and high,medium and low dose NaHS groups (NaHS1,NaHS2 and NaHS3 groups).The animals were anesthetized with intraperitoneal chloral hydrate.The focal cerebral ischemia was induced by middle cerebral artery occlusion.Normal saline 1 ml/kg was injected intraperitoneally at 3 h after the model was established.NaHS 2.8,1.4 and 0.7 mg/kg were injected intraperitoneally in NaHS1,NaHS2 and NaHS3 groups,respectively.At 24 h after the model was established,the cerebral infarct volume was determined.The changes in the cerebral infarct volume were observed after administration of NaHS.Cerebral specimens on the ischemic side were obtained for determination of the content of H2S and activity of 3-mercaptopyruvate sulphurtransferase (3MST) in brain tissues.The mitochondria were extracted for determination of the activity and swelling of mitochondrial membrane and changes in the total ATPase,superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities and malondialdehyde (MDA) content.Results Compared with group S,the cerebral infarct volume was significantly enlarged in CI,NaHS1,NaHS2 and NaHS3 groups,the content of H2 S in brain tissues and activity of mitochondrial 3MST were decreased in CI,NaHS2 and NaHS3 groups,the activities of mitochondria,SOD and GSH-Px were significantly decreased,and the swelling of mitochondrial membrane and content of MDA were increased in CI and NaHS3 groups,the total ATPase activity was decreased in CI group,and SOD activity was decreased in NaHS1 and NaHS2 groups.Compared with CI group,the cerebral infarct volume was significantly reduced,the content of H2 S in brain tissues and activity of mitochondrial 3MST were increased,the activities of mitochondria,total ATPase,SOD and GSH-Px were increased,the swelling of mitochondrial membrane was reduced,and the content of MDA was decreased in NaHS1 and NaHS2 groups.Conclusion The mechanism by which exogenous H2 S mitigates focal cerebral ischemia is related to enhanced anti-oxidant activity of mitochondria and reduced mitochondrial damage in rats.
