RGD Reference Report - Glutamine inhibits over-expression of pro-inflammatory genes and down-regulates the nuclear factor kappaB pathway in an experimental model of colitis in the rat.

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Glutamine inhibits over-expression of pro-inflammatory genes and down-regulates the nuclear factor kappaB pathway in an experimental model of colitis in the rat.
Authors:	Fillmann, H Kretzmann, NA San-Miguel, B Llesuy, S Marroni, N Gonzalez-Gallego, J Tunon, MJ
Citation:	Fillmann H, etal., Toxicology. 2007 Jul 17;236(3):217-26. Epub 2007 Apr 27.
RGD ID:	2298659
Pubmed:	PMID:17543437 (View Abstract at PubMed)
DOI:	DOI:10.1016/j.tox.2007.04.012 (Journal Full-text)
We investigated the effects of glutamine on markers of oxidative stress, nuclear factor kappaB (NF-kappaB) activation, and pro-inflammatory mediators in a rat model of experimental colitis induced by intracolonic administration of 7% acetic acid. Glutamine (25 mg/kg) was given by rectal route 48 and 24h before acetic acid instillation. Glutamine significantly reduced gross damage and histopathological scores, and partially prevented the decrease of anal pressure observed in the animals receiving acetic acid. Increases in the cytosolic concentration of TBARS and hydroperoxide-initiated chemiluminescence were significantly prevented in glutamine-treated animals. Acetic acid instillation induced a marked increase of the NF-kappaB p65 subunit expression in the nucleus and resulted in significant changes in the cytosolic protein level of IkappaB kinases (IKKalpha and IKKbeta) and the non-phosphorylated form of the inhibitor IkappaBalpha. Protein levels of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) were significantly increased. All these effects were partially prevented by administration of glutamine. It is concluded that the anti-inflammatory activity of glutamine in a rat model of acetic acid-induced colitis may be mediated, at least in part, by inhibition of the expression of certain pro-inflammatory mediators which are regulated by the oxidative stress-sensitive NF-kappaB signalling pathway.

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RGD Manual Disease Annotations Click to see Annotation Detail View

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Object Symbol	Species	Term	Qualifier	Evidence	With	Notes	Source	Original Reference(s)
CHUK	Human	colitis	treatment	ISO	Chuk (Rattus norvegicus)		RGD
Chuk	Rat	colitis	treatment	IEP			RGD
Chuk	Mouse	colitis	treatment	ISO	Chuk (Rattus norvegicus)		RGD
IKBKB	Human	colitis	treatment	ISO	Ikbkb (Rattus norvegicus)		RGD
Ikbkb	Rat	colitis	treatment	IEP			RGD
Ikbkb	Mouse	colitis	treatment	ISO	Ikbkb (Rattus norvegicus)		RGD
PTGS2	Human	colitis	treatment	ISO	Ptgs2 (Rattus norvegicus)		RGD
Ptgs2	Rat	colitis	treatment	IEP			RGD
Ptgs2	Mouse	colitis	treatment	ISO	Ptgs2 (Rattus norvegicus)		RGD

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Biological Process

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Object Symbol	Species	Term	Qualifier	Evidence	With	Notes	Source	Original Reference(s)
Chuk	Rat	response to acetate		IEP			RGD
Chuk	Rat	response to amino acid		IEP			RGD

Objects Annotated

Genes (Rattus norvegicus)

Chuk (component of inhibitor of nuclear factor kappa B kinase complex)

Ikbkb (inhibitor of nuclear factor kappa B kinase subunit beta)

Ptgs2 (prostaglandin-endoperoxide synthase 2)

Genes (Mus musculus)

Chuk (conserved helix-loop-helix ubiquitous kinase)

Ikbkb (inhibitor of kappaB kinase beta)

Ptgs2 (prostaglandin-endoperoxide synthase 2)

Genes (Homo sapiens)

CHUK (component of inhibitor of nuclear factor kappa B kinase complex)

IKBKB (inhibitor of nuclear factor kappa B kinase subunit beta)

PTGS2 (prostaglandin-endoperoxide synthase 2)

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Glutamine inhibits over-expression of pro-inflammatory genes and down-regulates the nuclear factor kappaB pathway in an experimental model of colitis in the rat.