Skin wound healing in the SKH‐1 female mouse following inducible nitric oxide synthase inhibition

Background  The inducible isoform of the nitric oxide (NO) synthase (NOS) enzyme (iNOS) is upregulated by inflammatory mediators and/or other pathological stresses, generating high, sustained levels of NO. Cumulative data suggest a role for NO in the regulation of skin wound healing, although it is not clear to what extent NO generated by iNOS, and possibly endothelial NOS (eNOS), contribute to that healing process. Because of the current lack of understanding regarding the contribution of iNOS in wound healing, as well as the lack of wound healing data available for SC‐842, an iNOS inhibitor, this in vivo study was conducted to investigate the possible role of SC‐842 in interfering with wound healing.

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