中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
Chinese Journal of Anesthesiology
2015年
7期
862-865
,共4页
自由基清除剂%休克,脓毒性%海马%细胞凋亡
自由基清除劑%休剋,膿毒性%海馬%細胞凋亡
자유기청제제%휴극,농독성%해마%세포조망
Free radical scavengers%Shock,septic%Hippocampus%Apoptosis
目的 评价依达拉奉对内毒素休克大鼠海马细胞凋亡的影响.方法 健康雄性SD大鼠36只,体重200～ 250 g,6周龄,采用随机数字表法,将其分为3组(n=12):对照组(C组)、内毒素休克组(ES组)和依达拉奉组(E组).ES组和E组股静脉注射LPS 10 mg/kg制备大鼠内毒素休克模型,C组给予等容量生理盐水.E组于造模成功后立即静脉注射依达拉奉3 mg/kg,每2h注射1次,直至处死;C组和ES组给予等容量生理盐水.每组分别于给予依达拉奉后6、12h时取6只大鼠,取海马,采用硫代巴比妥酸法测定丙二醛(MDA)含量,采用酶联免疫吸附法检测肿瘤坏死因子-α(TNF-α)及白细胞介素-6(IL-6)的含量;采用TUNEL法检测海马CA1区细胞凋亡情况,计算凋亡指数.结果 与C组比较,ES组和E组给予依达拉奉后6、12h时海马MDA、TNF-α和IL-6含量升高,给予依达拉奉后12h时凋亡指数升高(P＜0.05);与ES组比较,E组给予依达拉奉后6、12h时海马MDA、TNF-α和IL-6含量降低,给予依达拉奉后12h时凋亡指数降低(P＜0.05).结论 依达拉奉可减轻内毒素休克大鼠海马细胞凋亡,其机制与降低氧化应激反应及炎性反应有关.
目的 評價依達拉奉對內毒素休剋大鼠海馬細胞凋亡的影響.方法 健康雄性SD大鼠36隻,體重200～ 250 g,6週齡,採用隨機數字錶法,將其分為3組(n=12):對照組(C組)、內毒素休剋組(ES組)和依達拉奉組(E組).ES組和E組股靜脈註射LPS 10 mg/kg製備大鼠內毒素休剋模型,C組給予等容量生理鹽水.E組于造模成功後立即靜脈註射依達拉奉3 mg/kg,每2h註射1次,直至處死;C組和ES組給予等容量生理鹽水.每組分彆于給予依達拉奉後6、12h時取6隻大鼠,取海馬,採用硫代巴比妥痠法測定丙二醛(MDA)含量,採用酶聯免疫吸附法檢測腫瘤壞死因子-α(TNF-α)及白細胞介素-6(IL-6)的含量;採用TUNEL法檢測海馬CA1區細胞凋亡情況,計算凋亡指數.結果 與C組比較,ES組和E組給予依達拉奉後6、12h時海馬MDA、TNF-α和IL-6含量升高,給予依達拉奉後12h時凋亡指數升高(P＜0.05);與ES組比較,E組給予依達拉奉後6、12h時海馬MDA、TNF-α和IL-6含量降低,給予依達拉奉後12h時凋亡指數降低(P＜0.05).結論 依達拉奉可減輕內毒素休剋大鼠海馬細胞凋亡,其機製與降低氧化應激反應及炎性反應有關.
목적 평개의체랍봉대내독소휴극대서해마세포조망적영향.방법 건강웅성SD대서36지,체중200～ 250 g,6주령,채용수궤수자표법,장기분위3조(n=12):대조조(C조)、내독소휴극조(ES조)화의체랍봉조(E조).ES조화E조고정맥주사LPS 10 mg/kg제비대서내독소휴극모형,C조급여등용량생리염수.E조우조모성공후립즉정맥주사의체랍봉3 mg/kg,매2h주사1차,직지처사;C조화ES조급여등용량생리염수.매조분별우급여의체랍봉후6、12h시취6지대서,취해마,채용류대파비타산법측정병이철(MDA)함량,채용매련면역흡부법검측종류배사인자-α(TNF-α)급백세포개소-6(IL-6)적함량;채용TUNEL법검측해마CA1구세포조망정황,계산조망지수.결과 여C조비교,ES조화E조급여의체랍봉후6、12h시해마MDA、TNF-α화IL-6함량승고,급여의체랍봉후12h시조망지수승고(P＜0.05);여ES조비교,E조급여의체랍봉후6、12h시해마MDA、TNF-α화IL-6함량강저,급여의체랍봉후12h시조망지수강저(P＜0.05).결론 의체랍봉가감경내독소휴극대서해마세포조망,기궤제여강저양화응격반응급염성반응유관.
Objective To evaluate the effect of edaravone on apoptosis in hippocampal cells in a rat model of endotoxic shock.Methods Thirty-six male Sprague-Dawley rats, weighing 200-250 g, aged 6 weeks, were randomly divided into 3 groups (n=12 each) using a random number table: control group (group C), endotoxic shock group (group ES), and edaravone group (group E).Lipopolysaccharide 10 mg/kg was injected via the femoral vein to establish the model of endotoxic shock in ES and E groups, while the equal volume of normal saline was given in group C.In group E, edaravone 3 mg/kg was intravenously injected immediately after establishment of the model once every 2 h until the animals were sacrificed.The equal volume of normal saline was given instead of edaravone in C and ES groups.At 6 and 12 h after administration of edaravone, 6 rats in each group were sacrificed, and the hippocampi were isolated for determination of malondialdehyde (MDA) content (using thiobarbituric acid method) , tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) contents (using enzyme-linked immunosorbent assay), and cell apoptosis in hippocampal CA1 region (by TUNEL assay).The apoptotic index was calculated.Results Compared with group C, the MDA, TNF-α and IL-6 contents were significantly increased at 6 and 12 h after administration of edaravone, and the apoptotic index was increased at 12 h after administration of edaravone in ES and E groups.Compared with group ES, the MDA, TNF-α and IL-6 contents were significantly decreased at 6 and 12 h after administration of edaravone, and the apoptotic index was decreased at 12 h after administration of edaravone in group E.Conclusion Edaravone can reduce apoptosis in hippocampal cells, and the mechanism is associated with the reduced oxidative stress and inflammatory responses in a rat model of endotoxic shock.
