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机构地区:[1]辽宁医学院附属第一医院 [2]辽宁医学院附属第二医院 [3]辽宁医学院药理学教研室,锦州121000
出 处:《中国应用生理学杂志》2010年第1期82-85,共4页Chinese Journal of Applied Physiology
摘 要:目的:观测κ阿片受体激动对去甲肾上腺素诱导心肌肥大的抑制作用,并与哌唑嗪、心得安作用进行比较。方法:结晶紫染色法测心肌细胞增殖程度;Lowry法测心肌细胞蛋白含量;计算机图象分析系统测心肌细胞体积;[3H]-亮氨酸掺入法测心肌细胞蛋白合成。结果:①低血清环境下,NE明显诱导心肌细胞蛋白含量、蛋白合成及体积的增加,但对增殖无影响。②哌唑嗪和心得安单独作用部分抑制NE诱导的心肌肥大;联合作用则完全抑制。③U50488H明显抑制NE诱导的心肌肥大;其抑制程度与哌唑嗪和心得安联合作用类似,明显高于二者单独作用。结论:NE通过激动α1-和β-肾上腺受体途径诱导心肌肥大。κ阿片受体激动显著抑制NE诱导的心肌肥大,这可能与干预α1-AR和β-AR途径有关。Objective:To demonstrate the inhibitory effect of κ-opioid receptor activation by U50488H on hypertrophy induced by NE in cultured neonatal rat cardiac myocytes and compare its effect with that of prazosin and propranolol.Methods:The cellular proliferation was determined with crystal violet staining.The protein content was assayed with Lowry's method.The cardiomyocytes volumes were measured by computer photograph analysis system.The protein synthesis was assayed with [3H]-lencine incorporation method.Results:①NE significantly induced the increase of protein content,[3H]-leucine incorporation and cell size without a concomitant increase in cell number in low serum medium.②These responses were partially suppressed by prazosin or propranolol alone and completely abolished by both in combination.③U50488H significantly inhibited the NE-induced increase of protein content,[3H]-leucine incorporation and cell size.The inhibitory effects of U50488H on NE-induced cardiac hypertrophy were greater than either prazosin or propranolol,but comparable to combination of both.Conclusion:NE,acting via both α1-and β-adrenergic pathway,stimulates myocyte hypertrophy.Stimulating κ-opioid receptor significantly inhibits NE-induced cardiac hypertrophy,which may be related with α1-and β-adrenergic pathway.
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