Limits...
Catechin suppresses an array of signalling molecules and modulates alcohol-induced endotoxin mediated liver injury in a rat model.

Bharrhan S, Koul A, Chopra K, Rishi P - PLoS ONE (2011)

Bottom Line: Additionally, nitrite levels and lactate dehydrogenase activities were also significantly elevated on chronic alcohol consumption.Alcohol exposure also increased the number of micronucleated cells indicating that alcohol abuse may again be associated with the nuclear changes.Moreover, a remarkable decrease in the percentage of micronucleated cells was observed with catechin supplementation indicating an apparent protection against alcohol-induced toxicity.

View Article: PubMed Central - PubMed

Affiliation: Department of Microbiology, Basic Medical Sciences Block, Panjab University, Chandigarh, India.

ABSTRACT
Induction of nuclear factor kappa B (NF-κB)-mediated gene expression has been implicated in the pathogenesis of alcoholic liver disease through enhanced production of reactive oxygen species and pro-inflammatory mediators. The present study was carried out to investigate the role of catechin as a chain breaking inhibitor against experimental alcoholic liver injury. Rats were administered 35% v/v ethanol orally at a dose of 10 g/Kg/day for two weeks, followed by 14 g/Kg/day for 10 weeks. Catechin (50 mg/Kg) was co-supplemented after 4 weeks of alcohol treatment till the end of the dosing period. Following chronic alcohol exposure, rats developed endotoxemia and severe pathological changes in the liver such as pronounced fatty change, vacuolar degeneration and inflammation. These changes were accompanied by activation of NF-κB and induction of inflammatory and cytotoxic mediators leading to increased level of tumor necrosis factor-alpha, enhanced formation of malondialdehyde in the liver followed by drastic alterations in the hepatic antioxidant defense systems. Additionally, nitrite levels and lactate dehydrogenase activities were also significantly elevated on chronic alcohol consumption. Alcohol exposure also increased the number of micronucleated cells indicating that alcohol abuse may again be associated with the nuclear changes. Supplementation with catechin ameliorated the alcohol-induced liver injury by downregulating the endotoxin-mediated activation of initial signalling molecule NF-κB and further going downstream the signalling cascade including tumor necrosis factor-alpha, nitric oxide and reactive oxygen species and by enhancing the antioxidant profile. These observations correlated well with the histological findings. Moreover, a remarkable decrease in the percentage of micronucleated cells was observed with catechin supplementation indicating an apparent protection against alcohol-induced toxicity. These findings suggest that catechin may alleviate experimental alcoholic liver disease by suppressing induction of NF-κB, a key component of signalling pathway, thus forming a pharmacological basis for designing novel therapeutic agents against alcohol induced endotoxin-mediated liver injury.

Show MeSH

Related in: MedlinePlus

Effect of catechin on liver MDA levels in alcohol-administered rats.Values are expressed as mean ± S.D. of eight different observations. *p<0.001 vs. control and catechin (CT) per se; #p<0.001 vs. Alcohol (Alc).
© Copyright Policy
Related In: Results  -  Collection


getmorefigures.php?uid=PMC3108820&req=5

pone-0020635-g005: Effect of catechin on liver MDA levels in alcohol-administered rats.Values are expressed as mean ± S.D. of eight different observations. *p<0.001 vs. control and catechin (CT) per se; #p<0.001 vs. Alcohol (Alc).

Mentions: Chronic administration of alcohol led to an increase in hepatic MDA level (807.47±133.95 nanomoles/mg protein) compared to the control group (352.5±106.54 nanomoles/mg protein) indicating an enhancement in the lipid peroxidation potential of the liver (p<0.001) (Figure 5). Although this increase was more than two fold, catechin supplementation to ethanol-treated rats significantly attenuated the alcohol-induced increase (p<0.001) in the liver MDA levels (410.61±144.82 nanomoles/mg protein) as compared to the alcohol group.


Catechin suppresses an array of signalling molecules and modulates alcohol-induced endotoxin mediated liver injury in a rat model.

Bharrhan S, Koul A, Chopra K, Rishi P - PLoS ONE (2011)

Effect of catechin on liver MDA levels in alcohol-administered rats.Values are expressed as mean ± S.D. of eight different observations. *p<0.001 vs. control and catechin (CT) per se; #p<0.001 vs. Alcohol (Alc).
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3108820&req=5

pone-0020635-g005: Effect of catechin on liver MDA levels in alcohol-administered rats.Values are expressed as mean ± S.D. of eight different observations. *p<0.001 vs. control and catechin (CT) per se; #p<0.001 vs. Alcohol (Alc).
Mentions: Chronic administration of alcohol led to an increase in hepatic MDA level (807.47±133.95 nanomoles/mg protein) compared to the control group (352.5±106.54 nanomoles/mg protein) indicating an enhancement in the lipid peroxidation potential of the liver (p<0.001) (Figure 5). Although this increase was more than two fold, catechin supplementation to ethanol-treated rats significantly attenuated the alcohol-induced increase (p<0.001) in the liver MDA levels (410.61±144.82 nanomoles/mg protein) as compared to the alcohol group.

Bottom Line: Additionally, nitrite levels and lactate dehydrogenase activities were also significantly elevated on chronic alcohol consumption.Alcohol exposure also increased the number of micronucleated cells indicating that alcohol abuse may again be associated with the nuclear changes.Moreover, a remarkable decrease in the percentage of micronucleated cells was observed with catechin supplementation indicating an apparent protection against alcohol-induced toxicity.

View Article: PubMed Central - PubMed

Affiliation: Department of Microbiology, Basic Medical Sciences Block, Panjab University, Chandigarh, India.

ABSTRACT
Induction of nuclear factor kappa B (NF-κB)-mediated gene expression has been implicated in the pathogenesis of alcoholic liver disease through enhanced production of reactive oxygen species and pro-inflammatory mediators. The present study was carried out to investigate the role of catechin as a chain breaking inhibitor against experimental alcoholic liver injury. Rats were administered 35% v/v ethanol orally at a dose of 10 g/Kg/day for two weeks, followed by 14 g/Kg/day for 10 weeks. Catechin (50 mg/Kg) was co-supplemented after 4 weeks of alcohol treatment till the end of the dosing period. Following chronic alcohol exposure, rats developed endotoxemia and severe pathological changes in the liver such as pronounced fatty change, vacuolar degeneration and inflammation. These changes were accompanied by activation of NF-κB and induction of inflammatory and cytotoxic mediators leading to increased level of tumor necrosis factor-alpha, enhanced formation of malondialdehyde in the liver followed by drastic alterations in the hepatic antioxidant defense systems. Additionally, nitrite levels and lactate dehydrogenase activities were also significantly elevated on chronic alcohol consumption. Alcohol exposure also increased the number of micronucleated cells indicating that alcohol abuse may again be associated with the nuclear changes. Supplementation with catechin ameliorated the alcohol-induced liver injury by downregulating the endotoxin-mediated activation of initial signalling molecule NF-κB and further going downstream the signalling cascade including tumor necrosis factor-alpha, nitric oxide and reactive oxygen species and by enhancing the antioxidant profile. These observations correlated well with the histological findings. Moreover, a remarkable decrease in the percentage of micronucleated cells was observed with catechin supplementation indicating an apparent protection against alcohol-induced toxicity. These findings suggest that catechin may alleviate experimental alcoholic liver disease by suppressing induction of NF-κB, a key component of signalling pathway, thus forming a pharmacological basis for designing novel therapeutic agents against alcohol induced endotoxin-mediated liver injury.

Show MeSH
Related in: MedlinePlus