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目的:探讨过敏性气道炎症大鼠肺内VCAM-1表达和嗜酸细胞浸润,以及速激肽NK-1受体拮抗剂SR140333和地塞米松的可能调节方式.方法:致敏大鼠以1％卵白蛋白气雾吸入攻击后24小时,测定VCAM-1在不同组别大鼠肺内的表达和支气管周围嗜酸细胞浸润.抗原攻击前3天,每天2次腹腔注射SR140333(0.01,0.10mg/kg)或地塞米松(0.50mg/kg).结果:与未致敏大鼠相比VCAM-1在致敏大鼠肺内表达增加(P<0.05),预先用地塞米松处理可抑制其增加(P<0.05),SR140333无此作用(P>0.05).此外,抗原攻击致敏大鼠促使支气管周围嗜酸细胞浸润,但不能进一步增加VCAM-1的表达(P>0.05).SR140333抑制嗜酸细胞浸润(P<0.05),但不影响VCAM-1表达(P>0.05);地塞米松则抑制这两种反应(P<0.05).结论:VCAM-1表达在抗原致敏后增加,地塞米松和SR140333抑制大鼠过敏性气道炎症的机制可能不同.
OBJECTIVE: To investigate the expression of VCAM-1 and eosinophils in the lung of allergic airway inflammation rats and the possible regulation of NK1 receptor antagonist SR140333 and dexamethasone.Methods: The expression of VCAM-1 in the lungs of different groups and eosinophil infiltration in bronchioles were measured 24 hours after inhalation of 1% ovalbumin aerosol.The intraperitoneal injections of SR140333 (0.01, 0.10, mg / kg) or dexamethasone (0.50 mg / kg) .Results: Compared with non-sensitized rats, the expression of VCAM-1 increased in the lungs of sensitized rats (P <0.05) (P <0.05), but SR140333 had no effect (P> 0.05) .In addition, antigen challenge elicited eosinophilic infiltration around bronchus, but could not further increase the expression of VCAM-1 (P> 0.05) .SR140333 Inhibited eosinophil infiltration (P <0.05), but did not affect the expression of VCAM-1 (P> 0.05), while dexamethasone inhibited both responses (P <0.05) .Conclusion: The expression of VCAM- The mechanisms by which increased, dexamethasone and SR140333 inhibit allergic airway inflammation in rats may be different.