中文摘要：

目的研究半胱氨酰白三烯受体1（CysLT1）在支气管哮喘（哮喘）大鼠肺组织中的表达,探讨炎性因子IFN-γ是否参与调节哮喘大鼠肺组织CysLT1的表达。方法以卵清蛋白致敏激发制作大鼠哮喘模型,然后测定不同质量浓度组胺时大鼠呼吸道压力,再取其肺组织,采用免疫组织化学法、反转录-聚合酶链反应法检测IFN-γ干预前后哮喘大鼠肺组织中CysLT1 mRNA的表达。结果当各实验组大鼠吸入组胺质量浓度为0 mg·L^-1、10 mg·L^-1和20 mg·L^-1时,测得呼吸道阻力值,任意2组比较差异均有统计学意义（Pa〈0.01）;免疫组织化学（IHC）法检测正常对照组（N组）、哮喘模型组（A组）、哮喘鼠雾化吸入低剂量IFN-γ干预组（L组）及高剂量干预组（H组）的CysLTl阳性细胞表达计数分别为11.889±2.369、19.333±3.240、26.000±5.522、33.222±4.493,任意2组比较差异均有统计学意义（Pa〈0.01）;RT-PCR法检测N组、A组、L组及H组的CysLT1 mRNA/β-actin相对密度分别为0.218±0.050、0.323±0.084、0.447±0.083、0.670±0.108,任意2组比较差异均有统计学意义（Pa〈0.01）。结论高、低剂量IFN-γ均能上调CysLT1在哮喘大鼠肺组织的表达,其中炎性因子IFN-γ可能通过上调CysLT1的表达水平而参与哮喘的发生发展。

英文摘要：

Objective To investigate the expression of cysteinyl leukotriene receptor 1 （ CysLTI ） in lung tissue of asthmatic rats, and to explore interferon -T （IFN -γ）involving the modulation of CysLTl expression. Methods The asthmatic rats model were made by stimulating them with ovalbumin,then the rats airway pressure were measured when asthmatic rats inhaled different concentration histamine and the rats lung tissue were taken,The positive cells expression of CysLTI and CysLT1 mRNA in the lung tissue of asthmatic rats were detected by immu- nohistochemical method and reverse transcription - polymerase chain reaction. Results When asthmatic rats inhaled histamine 0 mg·L^-1, 10.0 mg·L^-1 and 20.0 mg·L^-1 ,the measured value was analyzed, the differences between every 2 groups were significant（ P 〈 0.01 ）. The positive expression of CysLT1 detected by IHC in the normal eonlxd group（ N greup）.,the asthmatic model group（ A group） ,the group of asthma rats that inhaled low dose IFN -γ（ L group） and the high dose group （H gro, up） were 11. 889 ± 2.369,19.333 ± 3. 240,26. 000 . 5. 522,33. 222 ±4.493 ,respectively ,the differences between every 2 groups were significant（ P, 〈 0.01 ） ;the relative intensity of CysLTI mR- NAγ - actin in N group, A group, L group, H groups were 0. 218 ± 0. 050,0. 323 ± 0. 084,0.447 ± 0. 083,0. 670 ± 0. 108, respectively. The differences between every 2 groups were significant （P 〈 0.01 ）. Conclusions IFN - γ can upregulate the expression of CysLT1 in lung of asthmatic rats, and with the greater dose the effect is stronger. IFN - γ may be involved in the origin and development of bronchial asthma by upregnlating the expression of CysLT1 in lung tissue.