Effects of quercetin on liver damage in rats with carbon tetrachloride-induced cirrhosis.
ABSTRACT Flavonoids are reported to exhibit a wide variety of biological effects, including antioxidant and free radical-scavenging activities. Evidence of oxidative reactions is often associated with various chronic disease processes characterized by accumulation of connective tissue. This study was aimed to investigate the protective effects of chronic administration of the flavonoid quercetin (150 micromol/kg body wt/day intraperitoneally) in rats with carbon tetrachloride-induced fibrosis. In animals rendered cirrhotic by administration of carbon tetrachloride for 16 weeks, cell necrosis, fibrosis, and inflammatory infiltration were found. Histological abnormalities were accompanied by a higher hepatic content of collagen and thiobarbituric acid-reactive substances. Expression of inducible nitric oxide synthase (iNOS) was significantly increased in the liver. Treatment with quercetin during 3 weeks improved liver histology and reduced collagen content, iNOS expression, and lipid peroxidation. Those effects were associated with an increased total peroxyl radical-trapping antioxidant capacity of liver. We conclude that quercetin is effective in this model of liver damage.
Article: Reversal of liver fibrosis.[show abstract] [hide abstract]
ABSTRACT: Hepatic fibrosis is a scarring process associated with an increased and altered deposition of extracellular matrix in the liver. It is caused by a variety of stimuli and if fibrosis continues unopposed, it would progress to cirrhosis which poses a significant health problem worldwide. At the cellular and molecular level, this progressive process is characterized by cellular activation of hepatic stellate cells and aberrant activity of transforming growth factor-beta with its downstream cellular mediators. Liver biopsy has been the reference test for assessment of hepatic fibrosis, but because of its limitations, noninvasive markers of liver fibrosis were developed. Liver fibrosis or cirrhosis was considered irreversible in the past but progress of research on the molecular pathogenesis of liver fibrosis has shown that hepatic cellular recovery is possible. Currently, no acceptable therapeutic strategies exist, other than removal of the fibrogenic stimulus, to treat this potentially devastating disease.Saudi Journal of Gastroenterology 02/2009; 15(1):72-9.
Article: Hepatic oxidative stress in an animal model of sleep apnoea: effects of different duration of exposure.[show abstract] [hide abstract]
ABSTRACT: Repeated apnoea events cause intermittent hypoxia (IH), which alters the function of various systems and produces free radicals and oxidative stress. We investigated hepatic oxidative stress in adult mice subjected to intermittent hypoxia, simulating sleep apnoea. Three groups were submitted to 21 days of IH (IH-21), 35 days of IH (IH-35), or 35 days of sham IH. We assessed the oxidative damage to lipids by TBARS and to DNA by comet assay; hepatic tissue inflammation was assessed in HE-stained slides. Antioxidants were gauged by catalase, superoxide dismutase, glutathione peroxidase activity and by total glutathione. After IH-21, no significant change was observed in hepatic oxidative stress. After IH-35, significant oxidative stress, lipid peroxidation, DNA damage and reduction of endogenous antioxidants were detected. In an animal model of sleep apnoea, intermittent hypoxia causes liver damage due to oxidative stress after 35 days, but not after 21 days.Comparative Hepatology 01/2011; 10(1):1. · 1.88 Impact Factor
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ABSTRACT: The use of carbon tetrachloride (CCl(4)) in rats is an experimental model of hepatic tissue damage; which leads to fibrosis, and at the long term, cirrhosis. Cirrhosis is the consequence of progressive continued liver damage, it may be reversible when the damaging noxae have been withdrawn. The aim of this study is to evaluate the changes caused by cirrhosis in lung and liver, through the experimental model of intraperitoneal CCI(4) administration. We used 18 male Wistar rats divided into three groups: control (CO) and two groups divided by the time of cirrhosis induction by CCI(4): G1 (11 weeks), G2 (16 weeks). We found significant increase of transaminase levels and lipid peroxidation (TBARS) in liver and lung tissue and also increased antioxidant enzymes SOD and CAT, as well as the expression of TNF-α and IL-1β in the lung of cirrhotic animals. We observed changes in gas exchange in both cirrhotic groups. We can conclude that our model reproduces a model of liver cirrhosis, which causes alterations in the pulmonary system that leads to changes in gas exchange and size of pulmonary vessels.Oxidative Medicine and Cellular Longevity 01/2012; 2012:486190.