【摘要】 目的研究大鼠左心室肌短暂外向钾电流(Ito)在糖尿病状态发生下降改变的分子机制。方法取体重150～200 g的雄性Sprague-Dawley大鼠,腹腔注射链脲菌素建立糖尿病大鼠模型,采用酶解法获得单个左室心外膜细胞,应用膜片钳全细胞方法记录Ito;用逆转录-聚合酶链式反应技术半定量编码该通道α亚单位mRNA的表达水平。结果与对照组相比,糖尿病大鼠左室心外膜细胞Ito密度显著降低,+60 mV时分别为27.38±1.16pA/pF(n=12)和16.85±2.31 pA/pF(n=25)(P<0.01);糖尿病大鼠左室心外膜肌细胞Ito通道α亚单位编码基因Kv4.2、Kv4.3 mRNA表达水平较对照组分别显著下调56.88%和46.57%;而Kv1.4 mRNA则较对照组上调约48.02%,三组基因表达水平的改变均具有显著性差异。结论糖尿病大鼠左心室肌外膜细胞Ito密度显著降低系编码该通道α亚单位的基因表达下调所致。更多还原

【Abstract】 Objective To investigate the molecular mechanism of transient outward potassium currents(Ito) decreasing in left ventricles from diabetic rats. Methods The diabetic model was established by injection of streptozocin peritoneally using male Sprague-Dawley rats weighing 150-200 g.Single myocytes of left ventricle epi were isolated by enzymatic perfusion.Ito was recorded with the whole-cell patch clamp technique,and then gene expressions of channel-forming subunits were evaluated by the technique of reverse transcript-poly.Results The Ito density(+60 mV)was significantly decreased in diabetic rats compared with controls[27.38±1.16 pA/pF(n=12) vs 16.85±2.31 pA/pF(n=25),P<0.01].The gene expression levels of Kv4.2 and Kv4.3 encoding α-subunit of Ito in diabetic rats were markedly decreased in contrast with those of controls by 56.88% and 46.57% respectively,while the level of Kv1.4 mRNA increased by 48.02% in diabetic group (P<0.01).Conclusion The decreased density of Ito in left ventricle epi of diabetic rats is mainly attributed to the down regulation of gene expressions of channel-forming α subunits.更多还原