Twenty Sprague-Dawley (SD) rats were randomly divided into normal control group and
COPD model group, with 10 rats in each group. The
COPD model was reproduced by
smoke inhalation and tracheal instillation of
lipopolysaccharide (LPS), and no such treatment was conducted in normal control group. Twenty-eight days after the model reproduction, the pulmonary function was determined, the pathological changes of lung tissue were observed with haematoxylin-
eosin (HE) staining,
interleukins (IL-6, IL-10) in serum were detected by
enzyme-linked
immunosorbent assay (ELISA), CD4⁺ CD25⁺ Foxp3⁺ Treg of peripheral blood was determined by flow cytometry, and the expressions of Foxp3, RORγt,
IL-17 protein in lung tissue were assayed by Western Blot.
RESULTS: Under light microscope, significal interstitial infiltration of inflammatory cells was found in alveoli and interstitial tissue of the lung, and destruction of alveolar tissue, alveolar wall thinning, and even
rupture to fuse into
bullae, and
bleeding into alveoli in different degress could be observed. Compared with the normal control group, forced vital capacity (FVC), forced expiratory volume in 0.3 second (FEV0.3), FEV0.3/FVC, peak expiratory flow (PEF) in model group were significantly decreased [FVC (mL): 8.04 ± 2.03 vs. 9.97 ± 2.14, FEV0.3 (mL): 6.16 ± 2.23 vs. 8.84 ± 2.12, FEV0.3/FVC: 0.70 ± 0.09 vs. 0.85 ± 0.11, PEF (mL/s): 33.56 ± 4.76 vs. 40.14 ± 5.64, P<0.05 or P<0.01]. Serum
IL-6 was obviously increased (ng/L: 93.17 ±20.96 vs. 76.28 ± 13.24, P<0.05),
IL-10 was significantly decreased (ng/L: 78.62 ± 15.17 vs. 104.34 ± 19.46, P<0.01), and CD4⁺ CD25⁺ FoxP3(+)Treg was significantly diminished [(2.75 ± 0.83)% vs. (4.16 ± 1.14)%, P<0.01] in model group compared with those in the normal control group. The expression of Foxp3
protein in lung tissue in model group was significantly down-regulated compared with that in the normal control group (gray scale: 0.38 ± 0.15 vs. 0.63 ± 0.11, P<0.01), and RORγt and
IL-17 protein expressions were significantly up-regulated [RORγt (gray scale): 0.96 ± 0.23 vs. 0.47 ± 0.11,
IL-17 (gray scale): 1.02 ± 0.24 vs. 0.34 ± 0.08, both P<0.01]. Correlation analysis showed that FEV0.3 was positively correlated with Foxp3 (r=0.585, P<0.05), and FEV0.3/FVC was negatively correlated with
IL-6 and RORγt (r=-0.655, r=-0.607, both P<0.05). PEF was positively correlated with Treg (r=0.573, P<0.05), and negatively correlated with
IL-17 (r=-0.198, P<0.05).
IL-6 was negatively correlated with Foxp3(r=-0.603, P<0.05),and positively correlated with RORγt (r=0.588, P<0.05).
IL-10 was positively correlated with Treg (r=0.573, P<0.05). Treg was positively correlated with Foxp3 (r=0.607, P<0.05), and negatively correlated with
IL-17 (r=-0.569, P<0.05). Foxp3 was negatively correlated with RORγt (r=-0.591, P<0.05). RORγt was positively correlated with
IL-17 (r=0.578, P<0.05).
CONCLUSIONS: