罗格列酮对哮喘患者T淋巴细胞PPAR-γ-核因子-κB通路的调控机制

摘要

目的：探讨罗格列酮对哮喘患者T淋巴细胞PPAR-γ-核因子-κB通路的调控机制。方法将10名哮喘患者外周血T淋巴细胞培养48 h,分哮喘未干预组、哮喘干预1组(在哮喘未干预组基础上在加终浓度为20μmol/L的罗格列酮)、哮喘干预2组(在哮喘未干预组基础上在加终浓度为20μmol/L的罗格列酮及终浓度为10μg/L的哮喘干预2组)。 ELISA法检测T淋巴细胞培养上清液中IL-10浓度,细胞免疫化学染色检测T淋巴细胞NF-κB活化率。结果 IL-10浓度：哮喘干预1组>哮喘未干预组>哮喘干预2组(均P<0．05)。 NF-κB活化率：哮喘未干预组>哮喘干预2组>哮喘干预1组(均P<0．05)。各组NF-κB活性分别与IL-10浓度成负相关。哮喘干预1组上清液中IL-10浓度明显高于哮喘未干预组,哮喘干预1组NF-κB活化率较哮喘未干预组及哮喘干预2组下降1倍,哮喘干预2组与哮喘未干预组NF-κB活化率相近, IL-10抗体可阻断罗格列酮对NF-κB活化率的抑制。结论罗格列酮对PPAR-γ-核因子-κB通路抑制作用与升高哮喘患者T淋巴细胞源性IL-10水平有关。%Objective To explore rosiglitazone regulation of PPAR-γ-NF-κB pathway derived from T-lym-phocytes in patients with asthma. Methods The T-lymphocytes from 10 patients with asthma were separated and T-lymphocytes in each group were cultured for 48 hours. T-lymphocytes were divided into four groups as following:pa-tients with asthma group, patients with asthma being cultured in rosiglitazone, patients with asthma being cultured in rosiglitazone and anti-IL-10. The level of IL-10 in supernatant liquid of cultured T-lymphocytes was detected by ELISA and the activities of NF-κB in T-lymphocytes of each group were detected by immunocy-tochemical stain. Re-sults The level of IL-10: patients with asthma being cultured in rosiglitazone patients with asthma group patients with asthma being cultured in rosiglitazone and anti-IL-10group (P<0. 05). The active rate of NF-κB was negatively correlated with the level of IL-10. Conclusion It is suggested that rosiglitazone can inhibit the PPAR-γ -NF-κB pathway in T-lymphocytes in patients with asthma by elevating production of IL-10.