Effect of inducible nitric oxide synthase on apoptosis in Candida-induced acute lung injury
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Excessive nitric oxide (NO) generated by inducible nitric oxide synthase (iNOS) aggravates acute lung injury (ALI) by producing peroxinitrite. We previously showed that the expression of iNOS and lung injury were suppressed by inhalation of a novel iNOS inhibitor, ONO-1714, in mice with <I>Candida</I>-induced ALI, and that nitric oxide produced by iNOS and apoptosis of epithelial cells were found to have a crucial role in <I>Candida</I>-induced ALI. In the present study, we investigated the effect of NO on the apoptosis of alveolar epithelial cells in <I>Candida</I>-induced ALI. Mice were pretreated by inhalation of ONO-1714 or saline (vehicle control of ONO-1714), and were given an intravenous injection of <I>Candida albicans</I> to induce ALI. After 24 h from injection of <I>Candida albicans</I>, we performed bronchoalveolar lavage and removed lung tissues. We assessed apoptosis on the basis of TUNEL staining and caspase 3 activity. Our results showed that apoptosis was suppressed by inhibition of iNOS-derived NO production by ONO-1714 inhalation. The augmented production of NO increased FasL, TNF-α, and mRNA production of Bax of lung that induced apoptosis of alveolar epithelial cells. Inhibition of iNOS-derived NO production by ONO-1714 inhalation ameliorated <I>Candida</I>-induced ALI and improved survival by suppressing apoptosis of alveolar epithelial cells.
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