| Objective To investigate the impact of Radix Astragali extract (RAE) and Astragalus polysaccharides (APS) against the damage of PM2.5 on alveolar macrophage (AM) phagocytosis from COPD mice.Methods 50 male mice were divided into COPD group, PM2.5 COPD group, RAE+PM2.5 COPD group, APS+PM2.5 COPD group aand normal control group. Mice of COPD groups were exposed to cigarette smoke for 90 days. The mice of PM2.5 COPD group were exposure to PM2.5 at nominal 770μg/m3 for 90 days, the mice of RAE+PM2.5 COPD group were fed with RAE (20g/kg) and exposure to PM2.5 at nominal 770μg/m3 for 90 days. The mice of APS+PM2.5 COPD group were fed with APS (200mg/kg) and exposure to PM2.5 at nominal 770μg/m3 for 90 days.Their lung function and morphology of brochus and lung tissue were observed. And their AMs were isolated after the end of cigarette smoke exposure. Flow cytometry method was applied to detect the ability of alveolar macrophages engulfed FITC-E. coli.The level of TAC, MDA and GSH-PX in lung tissue were measured by colorimetric analysis.Results (1) The results of pulmonary function tests and morphology of brochus and lung tissue:After exposure to cigarette smoke,the pulmonary function of PIF and PEF in The mice of COPD group (7.53±1.07), (4.41±0.47) were significantly lower than those from normal control group (11.65±1.27), (7.43±0.62) (all P<0.01). Those from PM2.5 COPD group (5.62±0.42), (3.09±0.21) were lower than those from COPD group (all P<0.01), Those from both RAE+P M2.5 COPD group (6.79±0.38), (3.99±0.26) and APS+PM2.5 COPD group (6.33±0.39), (3.61±0.23)were higher than those from PM2.5 COPD group (all P<0.01). Those from RAE+PM2.5 COPD group were higher than those from APS+PM2.5 COPD group (P<0.01). Significant small airway inflammation and emphysema were seen in the lung tissue of PM2.5 COPD group. while significant improvement were observed in RAE+PM2.5 COPD group and APS+PM2.5 COPD group when compared with PM2.5 COPD group.(2)The phagocytosis of alveolar macrophage:The percentage of positive cells and mean fluorescence intensity (MFI) from the mice of COPD group (4817±398), (30.66±2.95)% significantly decreased than those from normal control group (10267±1358), (69.04±5.43)% and (all P<0.01). Those from PM2.5 COPD group (3176±501),20.36±3.46)% decreased more than those from COPD group (all P<0.01). Both the mice of RAE+PM2.5 COPD group (4526±355), (29.1±1.93)% and the mice of APS+PM2.5 COPD group (4192±266), (26.48±3.06)% significantly decreased than those from PM2.5 COPD group (all P<0.01). The mice of RAE+PM2.5 COPD group decreased more than those from APS+PM2.5 COPD group (P<0.05).(3) The degree of oxidative stress:the level of TAC and GSH-PX in lung homogenates from the mice of COPD group (6.83±0.36), (46.49±2.59) were lower than those from normal control group (17.99±0.09), (84.32±5.65) and (all P<0.01). Those from PM2.5 COPD group (3.61±0.29), (32.36±3.78) were lower than those from COPD group (all P<0.01). Those from both RAE+PM2.5 COPD group (6.50±0.35), (44.22±3.15) and APS+PM2.5 COPD group (5.91±0.27), (40.21±1.93)were higher than those from PM2.5 group(all P<0.01). Those from RAE+PM2.5 COPD group were higher than those from APS+PM2.5 COPD group (all P<0.01). The content of MDA in lung homogenates in COPD group (2.73±0.22) were higher than those from normal control group (1.74±0.37) and (P<0.01). Those from PM2.5 COPD group (3.55±0.33) were higher than those from COPD group (P<0.01). Those from both RAE+PM2.5 COPD group (2.89±0.17) and APS+PM2.5 COPD group (3.06±0.15) were lower than those from PM2.5 group (all P<0.01). Those from RAE+PM2.5 COPD group were lower than those from APS+PM2.5 COPD group (P<0.05).(4) At basic status, positive correlations existed between MFI, phagocytic percentage and TAC (r=0.883,0.964,P<0.01,0.01), and GSH-PX (r=,0.897,0.896, P<0.01,0.01), while negative correlations between MFI, phagocytic percentage and MDA (r=-0.756,-0.908,P<0.05,0.01) in COPD mice after PM2.5 intervened. Positive correlations existed between MFI, phagocytic percentage and TAC (r=0.877,0.857, P<0.01,0.01), GSH-PX (r=0.901,0.795, P<0.01,0.01), while negative correlations between MFI, phagocytic percentage and MDA (r=-0.961,-0.722, P<0.01,0.05) in COPD mice after RAE+PM2.5 intervened. Positive correlations existed between MFI, phagocytic percentage and TAC (r=0.837,0.681, P<0.01,0.05), GSH-PX (r=0.780,0.831, P<0.01,0.01), while negative correlations between MFI, phagocytic percentage and MDA (r=-0.880,-0.761, P<0.01,0.05) in COPD mice after APS+PM2.5 intervened.Conclusions Phagocytosis of AMs from COPD mice was damaged, and the oxidant production from COPD mice was increased. Long-term exposure to PM2.5 also increased the damage of the phagocytosis of AMs from COPD mice, and facilitate oxidant production from COPD mice. RAE significantly decreased the damage of phagocytosis of AMs and reduced oxidant production more than APS from COPD mice after exposure to PM2.5. There is a Protection of RAE and APS gainst the damage of PM2.5 on AM phagocytosis from COPD mice, which is ralate to the reduction of oxidative stress. |
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