【摘要】 目的:探讨高血糖状态对大鼠骨骼肌和心肌C-Jun氨苯末端激酶(C-JunN-terminalkinase,JNK)和p38激酶活性的作用,进一步了解糖尿病的发病机制,为糖尿病的临床康复治疗提供一些理论依据。方法:12周龄、体质量200～230g的SD大鼠12只,根据是否注射链脲佐菌素(streptozotocin,STZ)随机分为高血糖组(n=6)和正常血糖组(n=6)。高血糖组大鼠腹腔内注射STZ(65mg/kg)建立持续高血糖模型(血糖>16mmol/L)。正常血糖组大鼠不注射STZ,维持正常血糖。运用化学发光法测定骨骼肌和心肌JNK和p38活性。结果:骨骼肌和心肌JNK活性在高血糖组明显增高,分别高于正常血糖组1.8倍和1.4倍。骨骼肌和心肌p38活性在高血糖组分别高于正常血糖组的2.0倍和1.6倍。结论:高血糖状态可以激活骨骼肌和心肌JNK和p38信号转导通道。提示细胞信号转导系统参与了糖尿病的发病机制。更多还原

【Abstract】 AIM:To explore the effects of C-JunN-term in al kinase(JNK)and p38stress activated protein kinases in rats my ocardial an d skeletal muscles under hy-perglycemia for comprehending the n osogenesis in o rder to and provide frames of reference for clinical dia betic rehabilitation.M ETHODS:In terms of whether Streptozotocin(STZ)was injected or not,twelve of Male Sprague-Dawley rats weighting 200-230g with 12weeks of age were r andomly divided into the fo llowing two groups:euglycemia grou p(n=6)and hy perglycemia group(n=6).Hyperglycemia group as blood glucose over 16mmol /L in animals was modeled by injection with STZ(65mg /kg).The rats of eug lycemia were managed by neither drug injection nor exercise.Activation of JNK a nd p38k inases in myocardial and skeletal muscle was measured by chemiluminesc ence method.RESULTS:JNK activity in hyperglycemia group increased significantl y to1.8times in skeletal muscle and 1.4t imes in myocardium comparing to e uglycemia group.Activity of p38in hyperglycemia group increased sign ifi-can tly in skeletal muscle(2times)and myocardium(1.6times)comparing to eugly cemia group.CONCLUSION:Hyperglycemia activates multiple intracellular signaling pathways of JNK and p38 in myocardial and skeletal muscle,suggesting that intracellular signaling pathways participate in pathological mechanism of di-abetes mellitus.更多还原