κ-阿片受体激动对高糖诱导心肌肥大的影响  

Effects of kappa-opioid recepter stimulation on high glucose induced myocardial hypertrophy of neonatal rats

作　　者：刘冬梅[1] 王洪新[1] 张蕾[1] 鲁美丽[1] 吴国强[1] 

机构地区：[1]辽宁医学院细胞生物学与新药开发重点实验室,锦州121001

出　　处：《中国应用生理学杂志》2010年第4期463-465,共3页Chinese Journal of Applied Physiology

基　　金：辽宁省自然科学基金资助项目(20082181)

摘　　要：目的:研究κ-阿片受体(κ-OR)激动剂U50488H在高浓度葡萄糖(25.5mmol/L)诱导的心肌细胞肥大中的作用及可能的信号转导通路。方法:以原代培养的新生大鼠心肌细胞为模型,应用25.5mmol/L的高浓度葡萄糖诱导心肌肥大,用Lowry法检测心肌细胞蛋白含量;用消化分离法及计算机图像分析系统检测心肌细胞体积;用Western蛋白印迹法测定细胞外信号调节激酶(ERK)磷酸化水平。结果:25.5mmol/L的高浓度葡萄糖使心肌细胞蛋白含量和体积明显增加,1μmol/L的U50488H能抑制高糖诱导的心肌肥大,使ERK磷酸化水平降低,与10μmol/L的ERK抑制剂U0126对心肌肥大的抑制程度相近,统计结果没有显著性差异。结论:U50488H抑制高糖诱导的心肌肥大与ERK信号有关。Objective：To observe the effects of kappa-opioid recepter stimulation on high glucose induced myocardial hypertrophy of neonatal rats. Methods： Using cultured myocardial cells as a model, the protein content was assayed with Lowrys method. The cardiomyocytes volumes were measured by computer photograph analysis system. The level of p-ERK44/42 was determined by Western blot. Results： Compared with the control, U50488H significantly inhibited the protein content and volumes of cultured hypertrophic myocardial cells induced by high glucose. Meanwhile the role of ERK was important. Conclusion： The stimulation of kappa-opiod can inhibit myocardial hypertrophy induced by high glucose, which is possibly via attenuating p-ERK.

关 键 词：受体 阿片样 κ 高糖 心肌肥大 

分 类 号：R335[医药卫生—人体生理学]