吸入一氧化氮对放射性肺纤维化中细胞因子及丝裂原物质变化的影响

EFFECT OF INHALED NITRIC OXIDE ON THE EXPRESSION OF RELATIVED CYTOKINES AND MITOGENS IN RADIATION PULMONARY FIBROSIS

观察了吸入NO对放射性肺纤维化中细胞因子及丝裂原物质表达变化的影响 ,以期对NO防治肺纤维化的可能机理进行探讨。6 0 Coγ射线照射Wistar大鼠建立放射性间质肺炎模型 ,分别在照射前 1d (B和C组 )以及照射后一个月 (D和E组 )开始吸入NO ,NO吸入浓度分别为2 0 μg·g- 1(B和D组 )和 1.0× 10 - 5μg·g- 1(C和E组 )。分别于照射后 1d、1周、1个月、3个月和 6个月取材应用免疫组化、原位杂交等方法检测TGFβ、ET - 1mRNA及其蛋白和TNFα、AII蛋白表达情况。结果表明 ,照射后大鼠肺脏TGFβ、ET - 1mRNA及其蛋白和TNFα、AII蛋白表达明显增强 ,照射前开始吸入NO组与正常大鼠相比前述各指标表达增强 ,但低于其它组。表明TGFβ、TNFα、ET - 1和AII均参与了放射性肺纤维化的病理发展过程 ,吸入NO可抑制上述因子的过度表达 ,从而减轻炎症 。

To investigate the Effect of inhaled Nitric Oxide on the expression of related cytokines and mitogens in radiation pulmonary fibrosis. Pulmonary fibrosis model was made induced by irradiation with 30Gy 60 Co γ rays on the whole thorax of Wistar rats. The NO inhalation started one day before (B and C groups) and one month (D and E groups) after radiation exposure respectively. The concentration of NO inhaled was 20μg·g -1 ppm (B and D groups) and 10μg·g -1 (C and E groups). Group A was not treated except for irradiation. The immunohistochemistry and in situ hybridization were examined in 1W, 1M, 3M, and 6M after radiation. In group A , the mRNA transcription of TGFβ and ET, and the protein expression of TGFβ, TNFα, ET and AII was increased significantly in group A after irradiation. In group B and C, the expression TGFβ, TNFα, ET and AII was higher than normal controls, but lower than that in other groups. TGFβ, TNFα and ET, AII are important factors in the formation of lung fibrosis, and NO has preventive and therapeutic effect through inhibiting the activities of these factors.