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

Effects of anisodamine on myocardial caspase-1 and interleukin-18 expression following overtraining-in- duced acute myocardial injury in rats

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200～220g，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，／Z=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20min腹腔注射山莨菪碱10mg／kg。ES组于力竭后即刻、6、24h时，AD组于力竭后6、24h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（cTnI）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。

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 intrapefitoneally 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 I （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 overtraininginduced 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.