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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(P<0.05),肺泡灌洗液中IL-10水平明显上升(P<0.05)、IL-17水平明显下降(P<0.05),血浆中IL-10含量无明显差异(P>0.05)、但IL-17水平有明显的下降(P<0.05)。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。
Objective To investigate the regulation of curcumin (CUR) on the expression of Th17 and Treg in rats with chronic obstructive pulmonary disease (COPD) and to explore its possible mechanism. Methods Thirty rats were randomly divided into three groups: normal control group, model group and CUR treatment group (200 mg / kg), 10 rats in each group. Adopting intratracheal instillation of lipopolysaccharide plus smoking combined modeling. The pathological changes in the lung tissue of rats were observed after the materials were taken from each group. The contents of CD4, CD25, Foxp3, Tregs in lung tissue were detected by enzyme linked immunosorbent assay (ELISA) Interleukin (IL) -10 and IL-17 were detected by immunohistochemistry. The expressions of CD4, CD25 and Foxp3 in lung tissue were detected by immunohistochemistry. Results Compared with the normal group, the levels of CD4, CD25 and Foxp3 regulatory T cells in the lung tissue of COPD rats were increased. Compared with the model group, the levels of CD4, CD25 and Foxp3 of the regulatory T cells in the CUR group were significantly decreased (P < (P <0.05). The level of IL-10 in bronchoalveolar lavage fluid was significantly increased (P <0.05), the level of IL-17 was significantly decreased (P < 17 levels decreased significantly (P <0.05). Conclusion CUR may play a protective and therapeutic role in COPD rats by regulating the balance of Th17 / Treg, increasing IL-10 and decreasing the content of IL-17 in COPD rats, decreasing CD4, CD25 and Foxp3 regulatory T cells.