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目的 :检测哮喘豚鼠气道上皮细胞Fas、NOS 2的表达 ,评价两者在哮喘发病机制中的作用。方法 :2 4只豚鼠随机分为 3组 :①哮喘组。用 10 %卵白蛋白 1ml腹腔注射致敏 ,2周后 ,用 1%卵蛋白超声雾化吸入 ,连续激发10次 ,复制豚鼠哮喘模型。②地塞米松 (Dxm)处理哮喘组。诱喘同哮喘组 ,在每次激发前 5min腹腔注射Dxm 0 .5mg/kg。③正常对照组。用生理盐水代替诱喘剂。应用免疫组化方法 (SP法 )检测气道上皮细胞Fas、NOS 2的表达。结果 :哮喘组豚鼠气道上皮细胞Fas的表达上调 [0 .2 2 37± 0 .0 32 4 ,与正常组 (0 .16 6 6± 0 .0 2 86 ) ,P <0 .0 0 1];Dxm促进Fas的表达 (0 .2 4 19± 0 .0 36 2 ,与正常组相比 ,P <0 .0 0 1;但与哮喘组相比 ,差别无显著性 ) ;正常对照组有较少的阳性表达。哮喘组豚鼠气道上皮细胞NOS 2的表达明显上调 (0 .2 5 6 7± 0 .0 345 ) ,Dxm组阳性信号稍弱 (0 .2 318± 0 .0 2 2 9) ,正常对照组有较少的阳性表达 (0 .182 9± 0 .0 2 5 9)。但哮喘组与Dxm组之间差别无显著性 (P >0 .0 5 )。哮喘豚鼠气道上皮细胞NOS 2、Fas的改变呈总体正相关 (r =0 .789,P <0 .0 1)。结论 :NOS 2为上皮损伤性因素 ,Fas可能为修复性因素。两者表达的同时上调说明气道上皮的损伤与修复同时进行
Objective: To detect the expression of Fas and NOS 2 in asthmatic guinea pig airway epithelial cells and to evaluate their roles in the pathogenesis of asthma. Methods: 24 guinea pigs were randomly divided into 3 groups: ① asthma group. The mice were sensitized by intraperitoneal injection of 10% ovalbumin (1 ml). After 2 weeks, they were inhaled with 1% ovalbumin by ultrasonic atomization, and the guinea pig asthma model was replicated 10 times. ② Dexamethasone (Dxm) treatment of asthma group. In the asthmatic group, Dxm 0.5 mg / kg was injected intraperitoneally 5 min before each challenge. ③ normal control group. Physiological saline was used instead of the anti-asthmatic agent. Immunohistochemistry (SP method) was used to detect the expression of Fas and NOS 2 in airway epithelial cells. Results: The expression of Fas in airway epithelial cells was increased in asthmatic guinea pigs [(0.227 ± 0.0304) vs. normal control (0.166 ± 0.2686, P <0.001) ]; Dxm promoted the expression of Fas (0.2419 ± 0.0362, P <0.001, compared with the normal group, but no significant difference compared with the asthma group); the normal control group Less positive expression. The expression of NOS 2 in asthmatic guinea pig airway epithelial cells was significantly increased (0. 2567 ± 0. 0 345), the positive signal in the Dxm group was weaker (0.2218 ± 0.229), the normal control group There was less positive expression (0.182 9 ± 0 .0259). However, there was no significant difference between the asthma group and the Dxm group (P> 0.05). The changes of NOS 2 and Fas in airway epithelial cells of asthmatic guinea pigs were positively correlated (r = 0.789, P <0.01). Conclusion: NOS 2 is an epithelial injury factor and Fas may be a repair factor. At the same time, the upregulation of both expression indicated that the injury and repair of airway epithelium were carried out at the same time