姜黄素对慢性阻塞性肺疾病大鼠辅助性T细胞17与调节性T细胞的调节作用

目的观察姜黄素(curcumin,CUR)对慢性阻塞性肺疾病(COPD)大鼠辅助性T细胞17(Th17)与调节性T细胞(Treg)的调节作用,探讨其可能作用机制。方法 30只大鼠随机分为3组:正常对照组、模型组、CUR治疗组(200 mg/kg),每组10只。采用气管内注射脂多糖叠加烟熏联合造模。各组处置取材后,观察大鼠肺组织病理变化;采用酶联免疫吸附法(ELISA)检测肺组织中调节性T细胞炎性标记物CD4、CD25、Foxp3的含量,大鼠外周血和BALF中白细胞介素(IL)-10、IL-17的浓度;免疫组化方法测定肺组织中CD4、CD25、Foxp3的表达。结果与正常组比较,COPD大鼠肺组织中的CD4、CD25、Foxp3调节性T细胞水平均升高;与模型组相比,CUR治疗组调节性T细胞CD4、CD25、Foxp3明显降低(P0.05),肺泡灌洗液中IL-10水平明显上升(P0.05)、IL-17水平明显下降(P0.05),血浆中IL-10含量无明显差异(P0.05)、但IL-17水平有明显的下降(P0.05)。结论 CUR可能通过调节COPD大鼠Th17/Treg平衡,升高IL-10及降低IL-17的含量,下调CD4、CD25、Foxp3调节性T细胞,从而发挥对COPD大鼠的保护和治疗作用。

Effect of curcumin on helper T cells 17 and regulatory T cells in rats with chronic obstructive pulmonary disease

Objective To observe the effect and mechanism of curcumin on helper T cells 17 (Th17) and regulatory T cells (Treg)in chronic obstructive pulmonary disease (COPD)rats.Methods A total 30 rats were randomly divided into normal group,model group and curcumin group at dose of 200 mg/kg (each n =10).COPD rat model was induced by intratracheal injection of lipopolysaccha-ride combined with smoke exposure.After removing rats’blocks of organs,the pathological changes of lung tissue were observed under microscope,the content of CD4,CD25 and Foxp3 in lung tissue were detected by using enzyme linked immunosorbent test (ELISA),IL-10 and IL-17 in peripheral blood and bronchoalveolar lavage fluid (BALF)were measured,and the expression of CD4,CD25 and Foxp3 were measured using immunohistochemistrical method.Results Compared with the normal group,the levels of CD4,CD25 and Foxp3 regulatory T cells in lung tissue of COPD rats increased significantly (P <0.05),and curcu-min reduced CD4,CD25,Foxp3 regulatory T cells level significantly (P <0.05 ),increased IL-10 in BALF(P <0.05 )and decreased IL-17 levels both in BALF and serum significantly (P <0.05 ). Conclusion The protective and therapeutic effect of curcumin on COPD rats may via the way of regula-ting the balance of Th17 and Treg,increasing content of IL-10 and decreasing content of IL-17,as well as downregulating CD4,CD25 and Foxp3.