Quercetin prevents oxidative stress and NF-kappaB activation in gastric
mucosa of portal hypertensive rats.
Moreira AJ, Fraga C, Alonso M, Collado PS, Zetller C, Marroni C, Marroni N,
Gonzalez-Gallego J.
Biochem Pharmacol 2004; 68(10):1939-46
Abstract
The present study was designed to investigate the effects of quercetin on
oxidative stress and activation of nuclear factor kappa B (NF-kappaB) in an
experimental model of portal hypertensive gastropathy induced by partial portal
vein ligation (PPVL). Portal pressure was significantly elevated in PPVL rats.
Transaminase and alkaline phosphatase activities were not significantly modified,
indicating absence of liver injury. Histological analysis of gastric sections
showed a lost of normal architecture, with edema and vasodilatation. The
cytosolic concentration of thiobarbituric acid reactive substances and the
lipoperoxidation measurement by chemiluminiscence were significantly increased.
Superoxide dismutase activity in gastric mucosa was significantly reduced.
Portal hypertensive gastropathy induced a marked activation of NF-kappaB,
accompanied by a decrease in IkappaB protein levels and a significant induction
of nitric oxide synthase (iNOS) protein. Administration of quercetin markedly
alleviated histological abnormalities and inhibited oxidative stress and NF-kappaB
activation. IkappaB decrease and induction of iNOS protein were partially
prevented by quercetin. Quercetin treatment, by abolishing the NF-kappaB signal
transduction pathway, may block the production of noxious mediators involved in
the pathogenesis of portal hypertensive gastropathy.
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