地塞米松快速抑制气道平滑肌细胞收缩的机制初探

目的通过对平滑肌细胞进行地塞米松快速预处理，拟证实糖皮质激素（glucocorticoids，GC）对气道平滑肌细胞内三磷酸肌醇（trisphosphate，IP3）和细胞内游离钙离子（[Ca^2＋]i）浓度升高有快速抑制作用。方法原代培养的大鼠气道平滑肌细胞，比较不同浓度地塞米松预处理后10min与对照组之间游离钙上升情况的区别。利用离子交换层析液闪法和Fura-2／AM显微荧光检测技术，分别检测肌IP3和[Ca^2＋]i在受到激动剂刺激后的浓度变化；同时设米非司酮（mifepristone，Ru486）及放线菌酮（cycloheximide，CHX）对照组，排除基因组作用在该反应中的影响。结果用GC温浴大鼠气道平滑肌细胞10min，能够明显降低刺激物引起的气道平滑肌细胞内IP3和[Ca^2＋]i峰值。以上反应均不能被RU486和CHX影响或者逆转。结论GC能够通过非基因组作用快速抑制刺激物引起的气道平滑肌的收缩反应，使细胞内IP3和[Ca^2＋]i浓度降低。GC对于气道平滑肌的收缩可能存在着快速抑制作用，并且这一作用是通过非基因组机制实现的。

Dexemisone rapid inhibitory effect and the possible mechanism on contraction of airway smooth muscle cells

Objective To prove glucocorticoids （GC） can affect the airway smooth muscle cells contraction by depreased the peaks of inositoI trisphosphate （IP3） and intracellular free calcium （[Ca^2＋ ]i） in the cells induced by agonist directly rapidly. Methods Pretreat the mice airway smooth muscle cells by dexamethasone （Dex） within 10 rain, test the peaks of IP3 and [Ca^2＋] i in the cells by treated with acetylcholine （Ach）. Results We found GC significantly decreased the and peaks of IP3 and [Ca^2＋ ]i elevation induced by agonist. Neither the glucocorticoid receptor antagonist mifepristone （RU486） nor the protein synthesis inhibitor cycloheximide （CHX） could alter the inhibitory effects of glucocorticoids stated above. Conclusions Our results demonstrate that GC exert rapid inhibitory effects on airway smooth muscle. The signal changes in this process that restrain the peask of [Ca^2＋ ]i may be responsible for the rapid nongenomic inhibitory effects of GC.