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To explore the effects of fine particulate matter on the level of nuclear factor erythroid-2 related factor 2 (Nrf2) in pulmonary tissues of chronic obstructive pulmonary disease (COPD) mouse models and its relationship with oxidative stress.Totally 40 BALB/c mice were randomly divided into normal control group, normal PM2.5 group, COPD control group and COPD PM2.5 group.COPD mice were established using exposure of cigarette smoking.PM2.5 (20 mg/kg) was intratracheally instilled in PM2.5 group mice.Mice pulmonary function was measured by mice noninvasive body plethysmograph and lung histopathology was observed in normal control group and normal PM2.5 group mice.The mRNA and protein expression of Nrf2 was measured with real-time polymerase chain reaction (PCR) and Western blot methods.Total antioxidative capacity (TAC) was measured by O-phenanthroline colorimetry.Glutathione peroxidase (GSH-PX) was measured by improved Hafeman colorimetry and malondialdehyde (MDA) by thiobarbiturieacid colorimetry.Nrf2 mRNA and protein in normal control group, normal PM2.5 group, COPD control group and COPD PM2.5 group were 1.00, 4.46±0.42, 4.93±0.63, 6.41±0.35 and 0.92±0.08, 1.23±0.07, 1.20±0.09, 1.43±0.10.Nrf2 mRNA and protein in COPD control group were increased than those in normal control group while those in normal PM2.5 group and COPD PM2.5 group were respectively higher than each control group.Comparing to normal PM2.5 group, the Nrf2 mRNA and protein in COPD PM2.5 group were increased (all P0.01). TAC and GSH-PX in each group were (5.1±0.4), (2.9±0.4), (3.3±0.3), (1.8±0.3) and (13.4±0.5), (9.9±0.7), (9.8±0.7), (7.0±0.6) U/mgpro.TAC and GSH-PX in COPD control group were decreased than those in normal control group while those in normal PM2.5 group and COPD PM2.5 group were respectively lower than each control group.Comparing to normal PM2.5 group, the Nrf2 mRNA and protein in COPD PM2.5 group were decreased (all P0.01). MDA in each group were (2.9±0.4), (4.8±0.5), (4.5±0.3), and (6.2±0.4) nmol/mgpro.MDA in COPD control group were increased than those in normal control group while those in normal PM2.5 group and COPD PM2.5 group were respectively higher than each control group.Comparing to normal PM2.5 group, the MDA in COPD PM2.5 group were increased (all P0.01). Positive correlations were observed between Nrf2 mRNA, protein and MDA, while negative correlations were observed between Nrf2 mRNA, protein and TAC, GSH-PX in all groups (all P0.05).PM2.5 can induce Nrf2 expression and aggravate oxidative stress in COPD mice.The increased expression of Nrf2 is closely associated with oxidative stress.

To investigate the inhibitory effects of codonopsis pilosula polysaccharides (CPP) on the deterioration of impaired phagocytosis of alveolar macrophage (AM) induced by fine particulate matter with a mean aerodynamic diameter ≤2.5 μm (PM2.5) in chronic obstructive pulmonary disease (COPD) mice.Sixty BALB/c male mice were randomly divided into control group, COPD group, PM2.5 group, PM2.5 COPD group, CPP COPD group and CPP+ PM2.5 COPD group. COPD mice were established using exposure of cigarette smoking. Meanwhile PM2.5 group, PM2.5 COPD group and CPP+ PM2.5 COPD group were exposed to PM2.5 (770 μg/m(3)) for 90 days. CPP COPD group and CPP+ PM2.5 COPD group were fed with CPP (300 mg/kg) for 90 days whilst other groups were fed with isovolumetric saline. After the models were established, mice peak inspiratory flow (PIF) and peak expiratory flow (PEF) were measured by noninvasive body plethysmograph and lung histopathology and mean linear intercept (MLI) were observed. AMs were isolated from lung tissue by discontinuous density gradient centrifugation. Mean fluorescence intensity (MFI) and the ability of AM phagocytosing flurescein isothiocyanate-labeled Escherichia coli (FITC-E.coli) (AM%) were detected by flow cytometry. Total antioxidative capacity (TAC) was measured by O-phenanthroline colorimetry. Malondialdehyde (MDA) was measured by thiobarbiturieacid colorimetry and glutathione peroxidase (GSH-PX) by improved Hafeman colorimetry.MFI in control group, COPD group, PM2.5 group, PM2.5 COPD group, CPP COPD group and CPP+ PM2.5 COPD group were 10 267±1 358, 4 817±399, 8 469±240, 3 176±501, 5 886±516 and 4 067±453. AM% in each group were (69.0±5.4)%, (30.7±3.0)%, (51.5±2.4)%, (20.4±3.5)%, (38.7±2.6)% and (28.7±4.3)%. MFI and AM% in COPD group and PM2.5 group were decreased than those in control group while those in PM2.5 COPD group were lower than in COPD group (all P0.01). Comparing to COPD group and PM2.5 COPD group respectively, MFI and AM% in CPP COPD group and CPP + PM2.5 COPD group were increased (all P0.01). TAC and GSH-PX in each group were (17.99±0.09), (6.83±0.36), (13.84±1.12), (3.61±0.29), (8.80±0.26), (5.43±0.30) U/mg protein and (84.3±5.7), (46.5±2.6), (62.0±2.2), (32.4±3.8), (53.4±4.0), (42.4±4.0) U/mg. TAC and GSH-PX in COPD group and PM2.5 group were lower than those from control group while those from PM2.5 COPD group were decreased than in COPD group (all P0.01). Comparing to COPD group and PM2.5 COPD group, TAC and GSH-PX in CPP COPD group and CPP+ PM2.5 COPD group were increased respectively (all P0.01). MDA in each group were (1.74±0.37), (2.73±0.22), (2.01±0.13), (3.55±0.33), (2.22±0.28) and (2.72±0.44) nmol/mg protein. MDA in COPD group and PM2.5 group were higher than that from control group while that from PM2.5 COPD group was higher than in COPD group; MDA in CPP COPD group and CPP+ PM2.5 COPD group were respectively decreased than those in COPD group and PM2.5 COPD group (all P0.05). Positive correlations were existed between MFI, AM% and TAC, GSH-PX, while negative correlations were existed between MFI, AM% and MDA in COPD group, PM2.5 group, PM2.5 COPD group, CPP COPD group and CPP+ PM2.5 COPD group.PM2.5 further impaired the defective phagocytosing capacity of AM and exacerbated oxidative stress in COPD mice. CPP can inhibit these effects. The protection of CPP may be closely related to its antioxidative effects.