Apocynin ameliorates endotoxin-induced acute lung injury in rats

• Apocynin attenuated LPS-induced ALI.
• It decreased total protein content, LDH activity and the accumulation of the inflammatory cells in BALF.
• Apocynin significantly increased SOD and GSH activities and decrease lung MDA content as compared to LPS group.
• Furthermore, it decreased pulmonary artery contraction induced by LPS.
• Apocynin upregulated mRNA expression of NFκBia, downregulated mRNA expression of TLR4 and decreased lung tissue inflammation.

Acute lung injury (ALI) is a serious clinical syndrome with a high rate of mortality. In this study, the effects of apocynin, a NADPH-oxidase (NOX) inhibitor on lipopolysaccharide (LPS)-induced ALI in rats were investigated. Male Sprague–Dawley rats were treated with apocynin (10 mg/kg) intraperitoneally (i.p.) 1 h before LPS injection (10 mg/kg, i.p.). The results revealed that apocynin attenuated LPS-induced ALI as it decreased total protein content, lactate dehydrogenase (LDH) activity and the accumulation of the inflammatory cells in the bronchoalveolar lavage fluid (BALF), In addition, apocynin significantly increased superoxide dismutase (SOD) and reduced glutathione (GSH) activities with significant decrease in the lung malondialdehyde (MDA) content as compared to LPS group in lung tissue and decreased pulmonary artery contraction induced by LPS. It also upregulated mRNA expression of inhibitory protein kappaB-alpha (NFκBia) and downregulated mRNA expression of Toll-Like receptor 4 (TLR4) and decreased inflammation observed in lung tissues.Collectively, these results demonstrate the protective effects of apocynin against the LPS-induced ALI in rats through its antioxidant and antiinflammatory effect that may be attributed to the decrease in mRNA expression of TLR4 and increasing that of NFκBia.