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- W2159049102 abstract "Hyperoxic exposures are often found in clinical settings of respiratory insufficient patients, although oxygen therapy (>50% O2) can result in the development of acute hyperoxic lung injury within a few days. Upon hyperoxic exposure, the inducible nitric oxide synthase (iNOS) is activated by a variety of proinflammatory cytokines both in vitro and in vivo. In the present study, we used a murine hyperoxic model to evaluate the effects of iNOS deficiency on the inflammatory response. Wild-type and iNOS-deficient mice were exposed to normoxia, 60% O2 or >95% O2 for 72 h. Exposure to >95% O2 resulted in an increased iNOS mRNA and protein expression in the lungs from wild-type mice. No significant effects of iNOS deficiency on cell differential in bronchoalveolar lavage fluid were observed. However, hyperoxia induced a significant increase in total cell count, protein concentration, LDH activity, lipid peroxidation, and TNF-α concentration in the bronchoalveolar lavage fluid compared to iNOS knockout mice. Moreover, binding activity of NF-κB and AP-1 appeared to be higher in wild-type than in iNOS-deficient mice. Taken together, our results provide evidence to suggest that iNOS plays a proinflammatory role in acute hyperoxic lung injury." @default.
- W2159049102 created "2016-06-24" @default.
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- W2159049102 date "2004-09-15" @default.
- W2159049102 modified "2023-10-15" @default.
- W2159049102 title "Proinflammatory role of inducible nitric oxide synthase in acute hyperoxic lung injury" @default.
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- W2159049102 doi "https://doi.org/10.1186/1465-9921-5-11" @default.
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