Original article can be found at: http://www.sciencedirect.com/science/journal/00243205 Copyright Elsevier Inc.We have investigated whether methylguanidine (MG), an uremic toxin, modulates the expression of the inducible nitric oxide synthase (iNOS) and nitric oxide (NO) release in vitro in LPS-induced J774 macrophages.Peer reviewe

Aucella

Berczi

Deakin

Deenitchina

Deschamps-Latscha

Drapier

Garcia-Valdecasas

Garreld

Girndt

Halwachs

Jones

Kawano

Kelly

Mendes-Ribeiro

Meur

Moncada

Orita

Ruetten

Shurtz-Swirski

Sorrentino

Yokozawa

Life Sciences

English

This study was performed in order to examine whether the uraemic toxin,
methylguanidine (MG), can modulate tumor necrosis factor alpha (TNF alpha)
release by activated macrophages. In this study we have evaluated the ability of 
MG to influence TNF alpha release in vitro, in Escherichia coli
lypopolysaccharide- (LPS)-stimulated J774 cells preincubated overnight with MG,
and in vivo in rats treated with MG before and after LPS challenge. Parallel
experiments employing N(G)-nitro-L-arginine methyl esther (L-NAME) were also
carried out for comparison. The effect of LPS (6 x 10(3) u/ml) on TNF alpha
release by J774, following overnight incubation with MG or L-NAME (1 mM), was
examined 3 hours after LPS challenge. LPS-stimulated J774 released 287.83+/-88
u/ml TNF alpha into the culture medium. MG (1 mM) significantly inhibited TNF
alpha release by 73% (P<0.05). L-NAME (1 mM) significantly inhibited TNF alpha
release too by 72.88% (P<0.05). The effect of MG and L-NAME have been also
studied in vivo. Serum TNF alpha levels in LPS treated rats 2 h after LPS
challenge were 88.33+/-31.7 u/ml as compared to the serum TNF alpha levels of
control rats (undetectable). Treatment of rats with MG (30 mg/kg, i.p.) strongly 
and significantly reduced TNF alpha release (98.71% inhibition; with P<0.001); in
the same experimental setting L-NAME (10 mg/kg, i.p.) also significantly reduced 
TNF alpha serum levels (76.47% inhibition; with P<0.01). These results could
indicate that immune disfunction related to uremia may be related to the
inhibitory capability of uremic catabolyte, MG, on TNF alpha synthesis and
release

Autore G

Marzocco S

Mirone VG

Baydoun A

Pinto A.

SORRENTINO, RAFFAELLA

Archivio della ricerca - Università degli studi di Napoli Federico II

In vitro and in vivo TNFalpha synthesis modulation by methylguanidine, an uremic catabolyte

We have investigated whether methylguanidine (MG), an uremic toxin, modulates the expression of the inducible nitric oxide synthase (iNOS) and nitric oxide (NO) release in vitro in LPS-induced J774 macrophages

Autore, G.

Marzocco, S.

Sorrentino, R.

Mirone, V. G.

Baydoun, A. R.

Pinto, A.

University of Hertfordshire Research Archive

In vitro and in vivo TNFa synthesis modulation by methylguanidine, an uremic catabolyte

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https://uhra.herts.ac.uk/id/eprint/800/1/900032.pdf

In vitro and in vivo TNFa synthesis modulation by methylguanidine, an uremic catabolyte

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Archivio della ricerca - Università degli studi di Napoli Federico II

University of Hertfordshire Research Archive

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