2007Clinical Education of General PracticeRequires access

Protective effects of dexamethasone on lipopolysaccharide induced lung injury in rats

Cheng Shuizhen

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Abstract

Objective To study the protective effects of dexamethasone on lipopolysaccharide(LPS)-induced lung injury in rats. Methods Seventy two S-D rats were randomly divided into 4 groups (group A, B, C, D), and each group divided into 3 subgroups at 1, 2 and 4 hours. Group D was control, group A received DEX (1mg/kg) by intraperitoneally injection, group B received LPS (5mg/kg) by intraperitoneally injection, and group C received DEX 1 hour before LPS by intraperitoneally injection. All the animals were killed with overdose of sodium pentathol at 1, 2 and 4 hours respectively. The bronchoalveolar lavage (BAL) was performed through a tracheal cannula with 8 ml ice-saline each rat, and the withdrawal rate of broncho alveolar lavage fluid (BALF) was more than 70%. The concentration of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and macrophage inflammatory protein-2 (MIP-2) were monitored in BALF by ELISA. Another 12 rats were randomly divided into 4 groups, 3 rats in each group for histological study. Results Lung injury was serious in group B compared with group D. There were no significant differences in the concentration of TNF-α, IL-1β and MIP-2 between group A and D ( P0.05). These parameters were significantly higher in group B and C than that of group A and D ( P0.05), and increased more significantly in group B( P0.05). The concentration of IL-1β and MIP-2 were increasing as the time elongation, and peaked at 4 hours; TNF-α peaked at 2 hours in these two groups . IL-1β , MIP-2 and TNF-α were significantly lower in group C than that of group B ( P0.05) . Conclusion Dexamethasone could protect LPS-induced lung injury through inhibit inflammatory mediators.

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Objective To study the protective effects of dexamethasone on lipopolysaccharide(LPS)-induced lung injury in rats. Methods Seventy two S-D rats were randomly divided into 4 groups (group A, B, C, D), and each group divided into 3 subgroups at 1, 2 and 4 hours. Group D was control, group A received DEX (1mg/kg) by intraperitoneally injection, group B received LPS (5mg/kg) by intraperitoneally injection, and group C received DEX 1 hour before LPS by intraperitoneally injection. All the animals were killed with overdose of sodium pentathol at 1, 2 and 4 hours respectively. The bronchoalveolar lavage (BAL) was performed through a tracheal cannula with 8 ml ice-saline each rat, and the withdrawal rate of broncho alveolar lavage fluid (BALF) was more than 70%. The concentration of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and macrophage inflammatory protein-2 (MIP-2) were monitored in BALF by ELISA. Another 12 rats were randomly divided into 4 groups, 3 rats in each group for histological study. Results Lung injury was serious in group B compared with group D. There were no significant differences in the concentration of TNF-α, IL-1β and MIP-2 between group A and D ( P0.05). These parameters were significantly higher in group B and C than that of group A and D ( P0.05), and increased more significantly in group B( P0.05). The concentration of IL-1β and MIP-2 were increasing as the time elongation, and peaked at 4 hours; TNF-α peaked at 2 hours in these two groups . IL-1β , MIP-2 and TNF-α were significantly lower in group C than that of group B ( P0.05) . Conclusion Dexamethasone could protect LPS-induced lung injury through inhibit inflammatory mediators.

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Available abstract

Objective To study the protective effects of dexamethasone on lipopolysaccharide(LPS)-induced lung injury in rats. Methods Seventy two S-D rats were randomly divided into 4 groups (group A, B, C, D), and each group divided into 3 subgroups at 1, 2 and 4 hours. Group D was control, group A received DEX (1mg/kg) by intraperitoneally injection, group B received LPS (5mg/kg) by intraperitoneally injection, and group C received DEX 1 hour before LPS by intraperitoneally injection. All the animals were killed with overdose of sodium pentathol at 1, 2 and 4 hours respectively. The bronchoalveolar lavage (BAL) was performed through a tracheal cannula with 8 ml ice-saline each rat, and the withdrawal rate of broncho alveolar lavage fluid (BALF) was more than 70%. The concentration of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and macrophage inflammatory protein-2 (MIP-2) were monitored in BALF by ELISA. Another 12 rats were randomly divided into 4 groups, 3 rats in each group for histological study. Results Lung injury was serious in group B compared with group D. There were no significant differences in the concentration of TNF-α, IL-1β and MIP-2 between group A and D ( P0.05). These parameters were significantly higher in group B and C than that of group A and D ( P0.05), and increased more significantly in group B( P0.05). The concentration of IL-1β and MIP-2 were increasing as the time elongation, and peaked at 4 hours; TNF-α peaked at 2 hours in these two groups . IL-1β , MIP-2 and TNF-α were significantly lower in group C than that of group B ( P0.05) . Conclusion Dexamethasone could protect LPS-induced lung injury through inhibit inflammatory mediators.

Key concepts: Medicine, Dexamethasone, Bronchoalveolar lavage, Saline, Lipopolysaccharide, Tumor necrosis factor alpha, Cannula, Group B

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