Estudios científicos

Resveratrol, a red wine polyphenol, attenuates lipopolysaccharide-induced oxidative stress in rat liver.

Abstract:

Lipopolysaccharide (LPS) is a glycolipid component of the cell wall of gram-negative bacteria inducing deleterious effects on several organs including the liver and eventually leading to septic shock and death. Endotoxemia-induced hepatotoxicity is characterized by disturbed intracellular redox balance, excessive reactive oxygen species (ROS) accumulation inducing DNA, proteins and membrane lipid damages. Resveratrol (trans-3,5,4' trihydroxystilbene) is a phytoalexin polyphenol exhibiting antioxidant and anti-inflammatory properties. In this study, we investigated the effect of subacute pre-treatment with this natural compound on LPS-induced hepatotoxicity in rat. Resveratrol counteracted LPS-induced lipoperoxidation and depletion of antioxidant enzyme activities as superoxide dismutase (SOD) and catalase (CAT) but slightly glutathione peroxidase (GPx) activity. The polyphenol also abrogated LPS-induced liver and plasma nitric oxide (NO) elevation and attenuated endotoxemia-induced hepatic tissue injury. Importantly resveratrol treatment abolished LPS-induced iron sequestration from plasma to liver compartment. Our data suggest that resveratrol is capable of alleviating LPS-induced hepatotoxicity and that its mode of action may involve differential iron compartmentalization via iron shuttling proteins. Copyright © 2010 Elsevier Inc. All rights reserved.

Comentarios divulgativos:

El lipopolosacárido es un compuesto glicolipídico de la pared de las bacterias gram- negativas el cual puede inducir en múltiples organismos incluyendo el hígado y ocasionalmente la muerte. El resveratrol es un polifenol que muestra propiedades antioxidantes y antinflamatorias. En este estudio se investigan los efectos del pretratamiento subcutaneo con este compuesto natural en LPS y su capacidad de inducir hepatotoxicidad en ratas. Los datos sugieren que el resveratrol es capaz de aliviar la hepatotoxicidad inducida por LPS.