地塞米松对哮喘动物模型支气管平滑肌MLCK表达的影响

目的观察地塞米松(DXM)对哮喘动物模型支气管平滑肌肌球蛋白轻链激酶(MLCK)表达的影响,探讨MLCK在哮喘发病中的作用。方法24只♂SD大鼠,随机等分为正常对照组、哮喘模型组和地塞米松组。以卵蛋白(OVA)诱发大鼠支气管哮喘模型。地塞米松组大鼠于每次激发前1h给予腹腔注射地塞米松0.5mg·kg-1。用免疫组织化学法和免疫印迹法分析三组大鼠支气管平滑肌中MLCK表达。结果免疫组织化学法分析显示DXM组大鼠支气管平滑肌MLCK的表达低于哮喘模型组(P<0.05),但与正常对照组比较差异无显著性(P>0.05)。同时,免疫印迹法检测也表明哮喘模型组大鼠smMLCK表达高于正常对照组及地塞米松组。结论MLCK参与支气管哮喘的发病,地塞米松通过下调哮喘大鼠支气管平滑肌MLCK表达,可能是糖皮质激素治疗哮喘的一种机制。

The effect of dexamethason on expression of myosin light chain kinase in bronchial smooth muscle of asthma animal model

Aim To investigate the effect of glucocorticoid -dexamethason (DXM) on the expression of myosin light chain kinase(MLCK) in brochial smooth muscle of asthma animal model and explore the role of MLCK in asthmatic pathogenesis.Methods Twenty-four male Sprague-Dawley(SD) rats were divided randomly into control group (n=8),asthmatic model group (n=8), and DXM group (n=8). Asthmatic model was established by sensitization and challenge with ovalbumin (OVA), control group with normal saline. One hour prior to OVA challenge, the DXM group rats were intraperitoneally injected with DXM 0.5 mg·kg -1. The expression of bronchial smooth muscle MLCK was detected by immunohistochemistry and Western-Bloting methods.Resutls The result analyzed by immunohistochemistry showed that the expression of MLCK in bronchial smooth muscle of DXM group rats decreased more significantly than that in asthmatic model group (P<0.05), while there was no significant difference between control group and DXM group(P>0.05). Meanwhile, Western-Bloting demonstrated that the expression of MLCK in bronchial smooth muscle increased more significantly in asthmatic model group than that in the other two groups.Conclusion MLCK was involved in the pathogenesis of asthma. Additionally, DXM may downregulate the expression of MLCK in bronchial smooth muscle to remit the attack of asthma, which may be one of mechanisms of glucocorticoid treating asthma.