Liver international : official journal of the International Association for the Study of the Liver · 2010
Antifibrotic and fibrolytic properties of celecoxib in liver damage induced by carbon tetrachloride in the rat.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Chávez Enrique, Segovia José, Shibayama Mineko, Tsutsumi Victor, Vergara Paula, Castro-Sánchez Luis, Salazar Eduardo Pérez, Moreno Mario G, Muriel Pablo
Аннотация
BACKGROUND: Transforming growth factor-beta (TGF-beta) plays a pivotal role in liver fibrosis, because it activates hepatic stellate cells, stimulating extracellular matrix deposition. Cyclooxygenase-2 (COX-2) has been associated with TGF-beta because its inhibition decreases TGF-beta expression and collagen production in some cultured cell types.
AIM: The aim of this work was to evaluate the ability of celecoxib (a selective COX-2 inhibitor) to prevent and to reverse the liver fibrosis induced by CCl(4).
METHODS: We established experimental groups of rats including vehicle and drug controls, damage induced by chronic CCl(4) administration and CCl(4) plus pharmacological treatment in both prevention and reversion models. We determined: alanine aminotransferase, alkaline phosphatase, gamma-glutamyl transpeptidase, COX and metalloproteinase-2 and -9 activities, lipid peroxidation, glutathione levels, glycogen and collagen content and TGF-beta expression.
RESULTS: Celecoxib prevented and aided to the recovery of livers with necrotic and cholestatic damage. Celecoxib exhibited anti-oxidant properties by restoring the redox equilibrium (lipid peroxidation and glutathione levels). Glycogen was decreased by CCl(4), while celecoxib partially prevented and reversed this effect. Celecoxib inhibited COX-2 activity, decreased TGF-beta expression, induced metalloproteinase-2 activity and, consequently, prevented and reversed collagen accumulation.
CONCLUSION: Our findings indicate that celecoxib exerts strong antifibrogenic and fibrolytic effects in the CCl(4) model of cirrhosis.
AIM: The aim of this work was to evaluate the ability of celecoxib (a selective COX-2 inhibitor) to prevent and to reverse the liver fibrosis induced by CCl(4).
METHODS: We established experimental groups of rats including vehicle and drug controls, damage induced by chronic CCl(4) administration and CCl(4) plus pharmacological treatment in both prevention and reversion models. We determined: alanine aminotransferase, alkaline phosphatase, gamma-glutamyl transpeptidase, COX and metalloproteinase-2 and -9 activities, lipid peroxidation, glutathione levels, glycogen and collagen content and TGF-beta expression.
RESULTS: Celecoxib prevented and aided to the recovery of livers with necrotic and cholestatic damage. Celecoxib exhibited anti-oxidant properties by restoring the redox equilibrium (lipid peroxidation and glutathione levels). Glycogen was decreased by CCl(4), while celecoxib partially prevented and reversed this effect. Celecoxib inhibited COX-2 activity, decreased TGF-beta expression, induced metalloproteinase-2 activity and, consequently, prevented and reversed collagen accumulation.
CONCLUSION: Our findings indicate that celecoxib exerts strong antifibrogenic and fibrolytic effects in the CCl(4) model of cirrhosis.
Предметные рубрики MeSH
Alanine TransaminaseAnimalsAnti-Inflammatory AgentsAntioxidantsAspartate AminotransferasesCarbon TetrachlorideCelecoxibChemical and Drug Induced Liver InjuryCollagenCyclooxygenase 2Cyclooxygenase 2 InhibitorsDisease Models, AnimalGlutathioneGlycogenLiverLiver CirrhosisMaleMalondialdehydeMatrix Metalloproteinase 2Matrix Metalloproteinase 9PyrazolesRatsRats, WistarSulfonamidesTime FactorsTransforming Growth Factor betagamma-Glutamyltransferase