[Inhibitory effects of codonopsis pilosula polysaccharides on the deterioration of impaired phagocytosis of alveolar macrophage induced by fine particulate matter in chronic obstructive pulmonary disease mice].
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OBJECTIVE
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.
METHODS
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.
RESULTS
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 P<0.01). 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 P<0.01). 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 P<0.01). 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 P<0.01). 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 P<0.05). 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.
CONCLUSIONS
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.
