PURPOSE: Hyperbaric oxygen (HBO) therapy has been suggested to palliate acute lung injury (ALI), but the mechanisms involved are not well understood. This study is to elucidate the involvement of AQP1 and AQP5 in the HBO related ALI therapy. MATERIALS AND METHODS: lipopolysaccharide (LPS) was administrated into SD rats to obtain ALI models. Pressure of oxygen (PaO2) and carbon dioxide (PaCO2) in arterial blood and oxygenation index in rats after LPS and HBO treatments were determined. Pathological changes of the lungs were examined by hematoxylin and eosin staining. Alteration of TNF-α level during LPS and HBO treatments was evaluated with ELISA analysis. Western blot was employed to assess the expression of AQP1 and AQP5. RESULTS: Blood gas indexes were largely decreased by LPS administration, which responded to HBO. Pathological examination showed that the inflammation symptoms in lungs induced by LPS were also palliated after HBO preconditioning. LPS induced the expression of TNF-α at a high level which could be downregulated by HBO and TNF-α antagonist treatments. Results of AQP1 and AQP5 determination found that HBO and TNF-α antagonist would upregulate the expression of AQP1 and AQP5 which was inhibited in rats with ALI. CONCLUSIONS: HBO therapy palliated LPS-induced ALI in rats by downregulating TNF-α expression. HBO also upregulated AQP1 and AQP5 expression. These results could serve as guidelines for the full understanding of ALI therapy by HBO, thus achieving maximized therapeutic efficiency.
PURPOSE: Hyperbaric oxygen (HBO) therapy has been suggested to palliate acute lung injury (ALI), but the mechanisms involved are not well understood. This study is to elucidate the involvement of AQP1 and AQP5 in the HBO related ALI therapy. MATERIALS AND METHODS:lipopolysaccharide (LPS) was administrated into SD rats to obtain ALI models. Pressure of oxygen (PaO2) and carbon dioxide (PaCO2) in arterial blood and oxygenation index in rats after LPS and HBO treatments were determined. Pathological changes of the lungs were examined by hematoxylin and eosin staining. Alteration of TNF-α level during LPS and HBO treatments was evaluated with ELISA analysis. Western blot was employed to assess the expression of AQP1 and AQP5. RESULTS: Blood gas indexes were largely decreased by LPS administration, which responded to HBO. Pathological examination showed that the inflammation symptoms in lungs induced by LPS were also palliated after HBO preconditioning. LPS induced the expression of TNF-α at a high level which could be downregulated by HBO and TNF-α antagonist treatments. Results of AQP1 and AQP5 determination found that HBO and TNF-α antagonist would upregulate the expression of AQP1 and AQP5 which was inhibited in rats with ALI. CONCLUSIONS: HBO therapy palliated LPS-induced ALI in rats by downregulating TNF-α expression. HBO also upregulated AQP1 and AQP5 expression. These results could serve as guidelines for the full understanding of ALI therapy by HBO, thus achieving maximized therapeutic efficiency.