[Molecular mechanisms of the iNOS regulation disorders in monocytes of patients with diabetic foot syndrome].
The activity of inducible synthase of nitrogen oxide (iNOS) and its modulators in vitro, while stimulation by lipopolysaccharides (LPS), was investigated in 36 patients with diabetic foot syndrome for the objective of complex estimation of monocytic functional state and its role in regulation of the cutaneous wound healing. The monocytic iNOS basal activity raising with simultaneous restriction of answering on LPS was noted. It was accompanied by enhancing of AT1-receptors sensitivity, as well as activity of proteinkinase C (PkC), phosphodiesterase (PHDE) and 5-lipoxigenase (5-LOG) on a background of cyclooxygenase (COG) activity lowering and significant inhibiting of proteinkinase A (PkA). Positive dynamics of the wound process was observed in 10 - 14 days, coexistent with the iNOS basal activity restriction. In the structure of answering on LPS there were noted significant reduction of 5-LOG/COG and PkC/PkA ratio, as well as PHDE activity and the AT1-receptors sensitivity lowering. But, even in case of the wound surface epithelization completion some disorders were saved in 24 - 30 days, causing support of the monocytes iNOS tolerance to LPS.
Barinov
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Sulaieva
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Barinova
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D000368:Aged; D001120:Arginine / Q000494:pharmacology; D002478:Cells, Cultured; D017719:Diabetic Foot / Q000097:blood* / Q000201:enzymology* / Q000473:pathology; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005260:Female; D006801:Humans; D008070:Lipopolysaccharides / Q000494:pharmacology; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000187:drug effects / Q000201:enzymology*; D009336:Necrosis; D009569:Nitric Oxide / Q000096:biosynthesis; D052247:Nitric Oxide Synthase Type II / Q000037:antagonists & inhibitors / Q000096:biosynthesis*
D004791:Enzyme Inhibitors; D008070:Lipopolysaccharides; D009569:Nitric Oxide; D001120:Arginine; C496319:NOS2 protein, human; D052247:Nitric Oxide Synthase Type II