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MPO — NOS2

Text-mined interactions from Literome

Konaka et al., J Physiol Pharmacol 1999 : This treatment also caused an increase of inducible NO synthase (iNOS) activity with the expression of its mRNA, myeloperoxidase (MPO) activity as well as thiobarbituric acid reactants ( TRBAS ) in the mucosa, and the changes in iNOS activity preceded those in MPO activity and TRBAS as well as lesion development
Ledbetter et al., Am J Vet Res 2001 : Cytotoxic effects of peroxynitrite, polymorphonuclear neutrophils, free-radical scavengers, inhibitors of myeloperoxidase , and inhibitors of nitric oxide synthase on bovine mammary secretory epithelial cells
Kumar et al., Nitric Oxide 2005 : Inducible nitric oxide synthase expression is inhibited by myeloperoxidase ... Here, we investigate the role of MPO in modulating the induction of iNOS by IFNgamma/LPS (IL)
Saed et al., Wound Repair Regen 2009 (Anoxia...) : Silencing iNOS reduced MPO and nitric oxide levels while silencing MPO had similar results, but to a lesser extent in both cell types
Wang et al., J Huazhong Univ Sci Technolog Med Sci 2010 (Anoxia...) : The MPO might be involved in the regulation of iNOS expression
Reino et al., PloS one 2011 (Lung Injury...) : Using C3H/HeJ mice that harbor a TLR4 mutation, we found that TLR4 activation was necessary for the development of T/HS porcine lymph induced lung injury as determined by Evan 's blue dye ( EBD ) lung permeability and myeloperoxidase (MPO) levels as well as the induction of the injurious pulmonary iNOS response
Hock et al., Immunology 2012 : This suppression was partially reversed by catalase addition ( P < 0·01 ) and largely reversed by addition of exogenous interleukin-2 ( P < 0·001 ) but was not significantly reduced by nitric oxide synthase inhibition, myeloperoxidase inhibition or addition of excess arginine
Tewari-Singh et al., PloS one 2012 (Inflammation) : In skin cells, silibinin ( 10 µM ) treatment 30 min after 0.35/0.5 mM CEES exposure caused a significant ( p < 0.05 ) reversal in CEES induced decrease in cell viability, apoptotic and necrotic cell death, DNA damage, and an increase in oxidative stress. Silibinin ( 1 mg ) applied topically to mouse skin 30 min post-CEES exposure ( 2 mg ), was effective in reversing CEES induced increases in skin bi-fold ( 62 % ) and epidermal thickness ( 85 % ), apoptotic cell death ( 70 % ), myeloperoxidase activity ( complete reversal ), induction of iNOS , COX-2, and MMP-9 protein levels ( > 90 % ), and activation of transcription factors NF-?B and AP-1 ( complete reversal )