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复制大鼠的慢性吸烟模型,采用气道反应性的测定、HE 染色、免疫组织化学染色、原位杂交和免疫印迹实验等方法,观察吸烟对大鼠支气管平滑肌大电导的钙激活的钾通道(BKca)和电压依赖性延迟整流钾通道Kv1.5 蛋白和mRNA表达的影响,以阐明吸烟引起的气道高反应性发病机制中钾通道表达变化的作用。结果显示:(1)慢性吸烟可降低大鼠大气道和小气道BKca 和 Kv1.5 蛋白和 mRNA 表达;(2)大气道 BKca 的降低程度大于 Kv1.5, 小气道 BKca 和 Kv1.5 的降低程度无明显差异;(3)吸烟对全肺组织BKca 和Kv1.5 的蛋白表达无明显影响。上述结果提示, 慢性吸烟可下调大鼠气道平滑肌钾通道BKca 和Kv1.5的表达水平, 是导致气道高反应的机制之一。
The model of chronic smoking in rats was replicated. The airway responsiveness, HE staining, immunohistochemical staining, in situ hybridization and western blotting were used to observe the effects of smoking on the calcium-activated potassium channel in rat bronchial smooth muscle BKca) and Kv1.5 protein and mRNA expression in voltage-dependent delayed rectifier potassium channel to elucidate the role of potassium channels in smoking-induced pathogenesis of hyperresponsiveness. The results showed that: (1) chronic smoking could decrease the expression of BKca and Kv1.5 protein and mRNA in the airway and small airway of rats; (2) the decrease of BKca in the airway was greater than that in Kv1.5 and the decrease of BKca and Kv1.5 (3) Smoking had no significant effect on the protein expression of BKca and Kv1.5 in the whole lung tissue. The above results suggest that chronic smoking can down-regulate the expression of BKca and Kv1.5 in the airway smooth muscle of rats, which is one of the mechanisms leading to airway hyperresponsiveness.