【摘要】 目的探讨地塞米松减轻哮喘气道炎症的作用及其分子机制。方法采用卵白蛋白致敏法建立豚鼠哮喘模型,以定喘止咳片做药物对照,治疗1周后记录各组的诱喘潜伏期,并进行肺组织病理学检查,同时分离BALF液中T淋巴细胞采用流式细胞仪定量检测方法(FITC-AnnexinV/PI染色法)测定其凋亡率。结果地塞米松能显著延长哮喘豚鼠的诱喘潜伏期、减轻气道炎症、促进BALF中T淋巴细胞的凋亡,作用明显优于定喘止咳片(P<0.05)。结论地塞米松有明确的抗炎平喘作用,促进气道T淋巴细胞凋亡可能为其主要的作用机制之一。更多还原

【Abstract】 Objective To observe the influence of Dexamethasone on airway inflammatory cellar infiltration and furtherly explore its molecular mechanism. Methods The asthma models of guinea pigs were established by ovalbumin sensitization. After one week for treatment, the incubation period of asthma was recorded. Then the pathologic histology of lung was observed and bronchoalveolar lavage (BAL) was performed. The apoptotic index of T lymphcytes isolated from BALF was analyzed by flow cytometry.[Rresults]:Dexamethasone could obviously prolong the incubation period of asthma, relieve airway inflammation, promote the apoptosis of T lymphcytes in airway, which effects were superior to that of Ding-chuan-zhi-ke-pian group (P <0.05). Conclusion The main mechanism of anti-inflammation of Dexamethasone may lie in promoting apoptosis of T lymphcytes in airway.更多还原