OBJECTIVE: To investigate the therapeutic effect of glucocorticoids on the acute pulmonary edema in rats induced by nitrogen dioxide (NO₂). METHODS: Thirty SD female rats were randomly equally divided into 5 groups: normal control group, NO₂ exposed group, high-, middle- and low-dose of glucocorticoids treated group (6 rats per group). 6 rats in the normal control group were exposed to room air for 30 min, and the other rats to NO₂. 18 rats in the glucocorticoids group were treated with different doses of dexamethasone (6.0, 3.0, 1.0 mg/kg), while the rats in the NO₂ poisoning group were treated with normal saline (2.5 mg/kg). The lung wet/dry (W/D) weight ratio was calculated, and plasma atrial natriuretic peptide (ANP) levels, superoxide dismutase (SOD) activity from whole blood, plasma interleukin 6 (IL-6), interleukin 10 (IL-10), tumor necrosis factor-α (TNF-α) and Interferon-γ (IFN-γ) were detected by enzyme-linked immunosorbent assay (ELISA). RESULTS: The lung W/D ratios were increased significantly in glucocorticoids treated group and NO₂-exposed group compared with normal control group (P < 0.05), while they were significantly reduced in glucocorticoids treated group as compared with NO₂-exposed group (P < 0.05). SOD activity in whole blood in glucocorticoids treated group and NO₂-exposed group was significantly lower than that of normal control group (P < 0.05), while it was no significant difference between that of glucocorticoids treated group and NO₂-exposed group (P > 0.05). Plasma ANP was significantly increased in NO₂-exposed group compared with normal control group (P < 0.05), while it was significantly decreased in glucocorticoids treated group compared with NO₂-exposed group (P > 0.05). Plasma TNF-α of high-, middle- and low-dose of glucocorticoids treated group [(27.04 ± 8.19), (40.10 ± 9.09), (39.76 ± 9.60) pg/ml] was decreased significantly as compared with NO₂-exposed group (68.55 ± 27.84 pg/ml) (P < 0.05). Plasma IL-6 in high- and middle-dose of glucocorticoids treated group [(15.97 ± 6.18), (19.69 ± 5.52) pg/ml] was significantly decreased as compared to NO₂-exposed group [(29.29 ± 9.31) pg/ml] (P < 0.05). Plasma IL-10 in high-, middle- and low-dose of glucocorticoids treated group [(23.24 ± 5.14), (27.78 ± 8.17), (33.29 ± 10.42) pg/ml] was significantly reduced compared with NO₂-exposed group [(44.38 ± 9.19) pg/ml] (P < 0.05). Plasma IFN-γ in high- and middle-dose of glucocorticoids treated group [(7.21 ± 4.55), (19.23 ± 4.35) pg/ml] was reduced compared with NO₂-exposed group [(30.83 ± 6.82) pg/ml] (P < 0.05). CONCLUSION: High-, middle-, low-dose glucocorticoids all can improve the permeability of alveolar wall and capillary, and have nonspecific anti-inflammatory effects. The therapeutic effects on pulmonary edema are significant. High and middle dose of glucocorticoids treated group are more useful for decreased inflammatory factors.
OBJECTIVE: To investigate the therapeutic effect of glucocorticoids on the acute pulmonary edema in rats induced by nitrogen dioxide (NO₂). METHODS: Thirty SD female rats were randomly equally divided into 5 groups: normal control group, NO₂ exposed group, high-, middle- and low-dose of glucocorticoids treated group (6 rats per group). 6 rats in the normal control group were exposed to room air for 30 min, and the other rats to NO₂. 18 rats in the glucocorticoids group were treated with different doses of dexamethasone (6.0, 3.0, 1.0 mg/kg), while the rats in the NO₂ poisoning group were treated with normal saline (2.5 mg/kg). The lung wet/dry (W/D) weight ratio was calculated, and plasma atrial natriuretic peptide (ANP) levels, superoxide dismutase (SOD) activity from whole blood, plasma interleukin 6 (IL-6), interleukin 10 (IL-10), tumor necrosis factor-α (TNF-α) and Interferon-γ (IFN-γ) were detected by enzyme-linked immunosorbent assay (ELISA). RESULTS: The lung W/D ratios were increased significantly in glucocorticoids treated group and NO₂-exposed group compared with normal control group (P < 0.05), while they were significantly reduced in glucocorticoids treated group as compared with NO₂-exposed group (P < 0.05). SOD activity in whole blood in glucocorticoids treated group and NO₂-exposed group was significantly lower than that of normal control group (P < 0.05), while it was no significant difference between that of glucocorticoids treated group and NO₂-exposed group (P > 0.05). Plasma ANP was significantly increased in NO₂-exposed group compared with normal control group (P < 0.05), while it was significantly decreased in glucocorticoids treated group compared with NO₂-exposed group (P > 0.05). Plasma TNF-α of high-, middle- and low-dose of glucocorticoids treated group [(27.04 ± 8.19), (40.10 ± 9.09), (39.76 ± 9.60) pg/ml] was decreased significantly as compared with NO₂-exposed group (68.55 ± 27.84 pg/ml) (P < 0.05). Plasma IL-6 in high- and middle-dose of glucocorticoids treated group [(15.97 ± 6.18), (19.69 ± 5.52) pg/ml] was significantly decreased as compared to NO₂-exposed group [(29.29 ± 9.31) pg/ml] (P < 0.05). Plasma IL-10 in high-, middle- and low-dose of glucocorticoids treated group [(23.24 ± 5.14), (27.78 ± 8.17), (33.29 ± 10.42) pg/ml] was significantly reduced compared with NO₂-exposed group [(44.38 ± 9.19) pg/ml] (P < 0.05). Plasma IFN-γ in high- and middle-dose of glucocorticoids treated group [(7.21 ± 4.55), (19.23 ± 4.35) pg/ml] was reduced compared with NO₂-exposed group [(30.83 ± 6.82) pg/ml] (P < 0.05). CONCLUSION: High-, middle-, low-dose glucocorticoids all can improve the permeability of alveolar wall and capillary, and have nonspecific anti-inflammatory effects. The therapeutic effects on pulmonary edema are significant. High and middle dose of glucocorticoids treated group are more useful for decreased inflammatory factors.