【摘要】 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.更多还原

【Abstract】 To determine vascular cell adhesion molecule-1 (VCAM-1) expression and eosinophil infiltration in the lungs of the rats with allergic airway inflammation, and their possible modulation by dexamethasone and neurokinin-1 receptor antagonist SR140333. METHODS: Sensitized rats were challenged with inhalation of 1 % ovalbumin aerosol. Protein expression of VCAM-1 in the lungs and eosinophil infiltration around bronchi in different groups were determined 24 h after challenge. SR140333 (0.01 and 0. 10 mg/kg) and dexamethasone (0.50 mg/kg) were injected ip, twice a day, for 3 d before challenge. RESULTS: The expression of VCAM-1 was increased in the sensitized rat lungs as compared with the non-sensitized rats (P <0.05). The increment was inhibited by pretreatment with dexamethasone (P <0.05), but not with SR140333 (P>0.05). On the other hand, antigen challenge in sensitized rats evoked eosinophil infiltration ( P < 0. 05) but no further increase in VCAM-1 expression (P>0.05). Furthermore, SR140333 inhibited eosinophil infiltration ( P <0.05) but had no effect on VCAM-1 expression ( P > 0. 05), whereas dexamethasone inhibited both responses (P<0.05). CONCLUSION: The expression of VCAM-1 increases during antigen sensitization in rat lungs, and dexamethasone and SR140333 may inhibit allergic airway inflammation in different mechanisms.更多还原