1,721,113 research outputs found
Tesi dottorato (Dr. Giuseppe Bianco) Vascular adaptation in spontaneously hypertensive rats during pregnancy
Tesi di dottorato ( Dr. ssa Stefania Marzocco) Studio di alcuni derivati guanidinici sull'attività della nitrossido sintasi inducibile
Enhancement by levamisole of the contractions induced by prostaglandin E2 in the guinea-pig isolated ileum.
Time related inhibition by methylguanidine in LPS-stimulated J774A.1 macrophages
Methylguanidine (MG) is a nitrogen compound deriving from protein catabolism that accumulates in
Chronic kidney disease (CKD). Changes in monocyte functions have been recognised as one of the most
important key factor responsible for the immunological disorders associated with uremia and it has been
demonstrated that high blood concentrations of nitrogen compounds, as MG, could be responsible of
immunodisfunctions associated to uremic syndrome. Inducibie nitric oxide synthase (iNOS) and
cycloxygenase-2 (COX-2) and their respective metabolites, nitric oxide and prostaglandins, are a crucial step
both in the activation of immunoresponsive cells and in the mechanism of citotoxicity, NO mediated. It has
been previously reported the ability of MG to inhibit iNOS activity and expression both in vitro and in vivo.
The aim of this study is to evaluate if MG could interfere with macrophagic immunoresponses also modulating
iNOS and COX-2 at different time of incubation in J774A.1 stimulated with Lipopolysahharide from E.coli.
Our results demonstrated that MG exerted inhibitory effect on iNOS and COX-2. These effects are related to
incubation time thus highliting the detrimental effect of immune system by MG in uremic conditions
Guanidino compounds inhibit nitric oxide release in J774A.1 macrophages
Chronic kidney disease (CKD) has been usually associated with accumulation of some nitrogen compounds deriving from protein catabolism like creatine (CRT), creatinine (CRTN), guanidine (GN) and methylguanidine (MG) proposed as responsible of some manifestations of uremic syndrome. Changes in monocyte functions have been recognised as one of the most important key factor responsible for the immunological disorders associated with uremia and it has been demonstrated that high blood concentrations of nitrogen compounds, as MG, could be responsible of immunodisfunctions associated to uremic syndrome. Nitric oxide (NO) production by inducibie nitric oxide synthase (iNOS) is a crucial step both in the activation of immunoresponsive cells and in the mechanism of citotoxicity NO mediated. The aim of this study is to evaluate if some uremic toxins like CRT, CRTN, GN, MG could interfere in macrophagic immunoresponse modulating iNOS activity. Our results demonstrated that GN and MG exerted the stronger effect in inhibiting NO release; this effect was reverted by a L-ARG supplementation. Moreover macrophage co-exposure to GN and MG further enhanced the inhibitory effect on iNOS activity and expression. Our results demonstrated that, among tested compounds, GN and MG significantly affected iNOS activity and expression
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