Abstract
Reactive oxygen species (ROS) are believed to play a key role in the induction of lung damage caused by pneumonia and therapeutic agents that could effectively scavenge ROS may prevent or reduce the deleterious effects of influenza-induced pneumonia. In this study, we first demonstrated that human catalase could attenuate acute oxidative injury in lung tissues following influenza-induced pneumonia. Mice were infected with influenza virus H1N1 (FM1 strain) and treated with recombinant human catalase (50,000 U/kg) by inhalation. The survival time and survival rates of H1N1 induced pneumonia mice were increased by treatment with recombinant human catalase. Protective efficacy of catalase was also observed in lung histology, anti-oxidant parameters, pulmonary pathology and influenza viral titer in lungs in mice. These observations were associated with increased serum superoxide and hydroxyl radical anion scavenging capacities. This study strongly indicated that recombinant catalase might be a potential therapy for H1N1 influenza-induced pneumonia.
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