摘要
目的观察地塞米松对哮喘豚鼠体外不同密度嗜酸粒细胞(EOS)凋亡及IL-3、IL-5和粒细胞-巨噬细胞集落刺激因子受体的共同β受体(βcR)mRNA表达的影响,探讨地塞米松促进哮喘EOS凋亡的机制。方法卵蛋白激发哮喘豚鼠动物模型48h后行支气管肺泡灌洗,分离低密度EOS(HEOS)及正常密度EOS(NEOS)。HEOS及NEOS分别与地塞米松(10^-1~10^-5mol/L)共培养24h,以原位杂交方法检测不同密度EOS的βcR mRNA表达,3′末端脱氧核苷转移酶介导的脱氧三磷酸尿苷缺口末端标记法检测细胞凋亡。结果地塞米松干预24h后,可见EOS凋亡增加的同时,不同密度EOS中βcR mRNA表达下降,并与地塞米松浓度呈剂量依赖性。βcR表达与EOS凋亡呈负相关(P〈0.05)。结论地塞米松可抑制不同密度EOS表达βcR,抑制其细胞因子活动,促进EOS凋亡。地塞米松可以通过增加EOS中βcR表达调节EOS凋亡。
Objective To investigate the effects of dexamethasone on expression of common β receptor (βcR) mRNA of interleukin (IL)-3, IL-5, GM-CSF receptors and apoptosis in eosinophils (EOS) of bronchoalveolar lavage fluid(BALF) in asthmatic guinea pig,and mechanism of dexamethasone promoting EOS apoptosis. Methods After guineas pigs were stimulated by ovalbumin for 48 hours,hypodense EOS and normodense EOS were purified from BALF by gradients of percoll. EOS were cultured in PRMI1640 medium. Dexamethasone (10^-1-10^-5 mol/L) was added in the wells. The mRNA expression of βcR in EOS was measured by hybridization. Apoptosis was detected by TdT-mediated dUTP nick end labeling. Results EOS cultured under the condition of dexamethasone administration in vitro, apoptotic EOS increased, βcR mRNA expression decreased in a close-dependent manner. There was significant negative correlation between EOS apoptosis and βcR mRNA expression. Conclusions Dexamethasone promotes EOS apoptosis,decreases expression of βcR in dose-dependent manner in vitro. βcR might be one of mechanisms that dexamethasone promotes apoptosis of EOS.
出处
《国际呼吸杂志》
2009年第4期197-200,共4页
International Journal of Respiration