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The efficacy of apocynin in mitigating LPS‐induced acute lung injury when given prior to, but not after LPS insult (660.3)

Apocynin (4‐hydroxy‐3‐methoxyacetophenone; APO) is an inhibitor of NADPH oxidase (NOX2) activation and a possible scavenger of reactive O2 species (ROS). Regulating NOX2 may play a crucial role in LPS (lipopolysacharide)‐induced ROS production and the pathogenesis of ALI. To evaluate the effect of APO on lung injury in mice following intra‐tracheal infusion of LPS (0111:B4 from E. coli) at 1 mg/kg, mice received iv APO at 2.5 mg/kg at 0.5h prior to LPS or 2h post LPS. Measurements were performed 24h post LPS. LPS significantly increased lung infiltration with inflammatory cells, lung alveolar‐capillary permeability (lung wet to dry ratio, leakage of protein and FITC‐dextran into the bronchoalveolar lavage fluid), expression of pro‐inflammatory cytokines (IL‐6, TNF‐α) and a chemokine (MIP‐2). APO dramatically reduced all of these parameters when administered at 0.5h prior to LPS but had no significant effect when administered at 2h post LPS. Thus, APO when administered prophylactically prevented lung inflammation, excessive ROS production, and cell injury but was not effective when administered during the early stages of LPS‐induced inflammation. These findings contrast with the recently reported effectiveness of MJ33, also an inhibitor of NOX2 activation, when administered 2 h post LPS. The mechanism for the difference between the 2 inhibitors requires further investigation.