中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2012年
2期
211-213
,共3页
李圣洪%张煜东%郭谦%韩霜%岳立辉%容俊芳
李聖洪%張煜東%郭謙%韓霜%嶽立輝%容俊芳
리골홍%장욱동%곽겸%한상%악립휘%용준방
山莨菪碱%运动过度%心肌疾病%半胱氨酸天冬氨酸蛋白酶1%白细胞介素18
山莨菪堿%運動過度%心肌疾病%半胱氨痠天鼕氨痠蛋白酶1%白細胞介素18
산랑탕감%운동과도%심기질병%반광안산천동안산단백매1%백세포개소18
ANISODAMINE%Hyperkinesis%Cardiomyopathies%Caspase 1%Interleukin-18
目的 评价山莨菪碱对过度训练致急性心肌损伤大鼠caspase-1和IL-18表达的影响.方法 健康雄性Wistar大鼠48只,体重200~ 220 g,采用随机数字表法,将其随机分为3组:对照组(C组,n=8)、力竭运动组(ES组,n=24)和山莨菪碱组(AD组,n=16).采用游泳力竭法建立过度训练致大鼠急性心肌损伤模型.AD组于力竭运动前20 min腹腔注射山莨菪碱10 mg/kg.ES组于力竭后即刻、6、24 h时,AD组于力竭后6、24 h时分别随机取8只大鼠,采集下腔静脉血样,采用ELISA法检测血清心肌肌钙蛋白I(cTnl)浓度,随后处死大鼠取心肌组织,采用免疫组化法检测caspase-1及IL-18的表达水平,光镜下观察病理学结果.结果 与C组比较,ES组各时点血清cTnI浓度升高,心肌组织caspase-1和IL-18表达上调(P<0.05);与ES组比较,AD组各时点血清cTnI浓度降低,心肌组织caspase-1和IL-18表达下调(P<0.05).AD组心肌病理学损伤程度轻于ES组.结论 山莨菪碱可减轻过度训练致大鼠急性心肌损伤,其机制与下调心肌组织caspase-1及IL-18表达有关.
目的 評價山莨菪堿對過度訓練緻急性心肌損傷大鼠caspase-1和IL-18錶達的影響.方法 健康雄性Wistar大鼠48隻,體重200~ 220 g,採用隨機數字錶法,將其隨機分為3組:對照組(C組,n=8)、力竭運動組(ES組,n=24)和山莨菪堿組(AD組,n=16).採用遊泳力竭法建立過度訓練緻大鼠急性心肌損傷模型.AD組于力竭運動前20 min腹腔註射山莨菪堿10 mg/kg.ES組于力竭後即刻、6、24 h時,AD組于力竭後6、24 h時分彆隨機取8隻大鼠,採集下腔靜脈血樣,採用ELISA法檢測血清心肌肌鈣蛋白I(cTnl)濃度,隨後處死大鼠取心肌組織,採用免疫組化法檢測caspase-1及IL-18的錶達水平,光鏡下觀察病理學結果.結果 與C組比較,ES組各時點血清cTnI濃度升高,心肌組織caspase-1和IL-18錶達上調(P<0.05);與ES組比較,AD組各時點血清cTnI濃度降低,心肌組織caspase-1和IL-18錶達下調(P<0.05).AD組心肌病理學損傷程度輕于ES組.結論 山莨菪堿可減輕過度訓練緻大鼠急性心肌損傷,其機製與下調心肌組織caspase-1及IL-18錶達有關.
목적 평개산랑탕감대과도훈련치급성심기손상대서caspase-1화IL-18표체적영향.방법 건강웅성Wistar대서48지,체중200~ 220 g,채용수궤수자표법,장기수궤분위3조:대조조(C조,n=8)、력갈운동조(ES조,n=24)화산랑탕감조(AD조,n=16).채용유영력갈법건립과도훈련치대서급성심기손상모형.AD조우력갈운동전20 min복강주사산랑탕감10 mg/kg.ES조우력갈후즉각、6、24 h시,AD조우력갈후6、24 h시분별수궤취8지대서,채집하강정맥혈양,채용ELISA법검측혈청심기기개단백I(cTnl)농도,수후처사대서취심기조직,채용면역조화법검측caspase-1급IL-18적표체수평,광경하관찰병이학결과.결과 여C조비교,ES조각시점혈청cTnI농도승고,심기조직caspase-1화IL-18표체상조(P<0.05);여ES조비교,AD조각시점혈청cTnI농도강저,심기조직caspase-1화IL-18표체하조(P<0.05).AD조심기병이학손상정도경우ES조.결론 산랑탕감가감경과도훈련치대서급성심기손상,기궤제여하조심기조직caspase-1급IL-18표체유관.
Objective To investigate effects of anisodamine on myocardial caspase-1 and interleukin-18 expression following overtraining-induced acute myocardial injury in rats.Methods Forty-eight male Wistar rats weighing 200-220 g were randomly divided into 3 groups:group control (group C,n =8) ; group exhausting swim (group ES,n =24) and group anisodamine (group AD,n =16).The animal model of overtraining-induced acute myocardial injury was developed by exhausting swim The animals were forced to swim until they were exhausted.The animals sank to the bottom and no righting reflex or escape response was elicited when they were taken out of water in groups ES and AD.In group AD anisodamine 10 mg/kg was given intraperitoneally 20 min before overtraining.Blood samples were taken from inferior vena cava immediately (T1) and at 6 and 24 h after overtraining (T2,T3 ) in group ES and at T2,T3 in group AD for determination of serum cardiac troponin 1 (cTnI) concentration (by ELISA).The animals were sacrificed after blood sampling and myocardial specimens were obtained for microscopic examination and determination of caspase-1 and interleukin-18 expression (by immuno-histochemistry).Results Overtraining significantly increased serum cTnI concentration and up-regulated myocardial caspase-1 and interleukin-18 expression in group ES as compared with group C.Anisodamine significantly attenuated overtraining-induced increase in serum cTnI concentration and myocardial caspase-1 and interleukin-18 expression in group AD as compared with group ES.Conclusion Anisodamine can reduce overtraining-induced acute myocardial injury by down-regulating caspase-1 and interleukin-18 expression.