TY - JOUR
T1 - Coffee prevents CCl4-induced liver cirrhosis in the rat
AU - Moreno, Mario G.
AU - Chavez, Enrique
AU - Aldaba-Muruato, Liseth R.
AU - Segovia, Jose
AU - Vergara, Paula
AU - Tsutsumi, Vìctor
AU - Shibayama, Mineko
AU - Rivera-Espinoza, Yadira
AU - Muriel, Pablo
N1 - Funding Information:
Acknowledgements The authors express their gratitude to Mr. Benjamín Salinas Hernández, Mr. Ramón Hernández, Q.F.B. Silvia Galindo, and M.V.Z. Ricardo Gaxiola for their excellent technical assistance. Enrique Chávez was a fellow of Conacyt. This work was supported in part by Conacyt grant 54756 (JS).
PY - 2011/9
Y1 - 2011/9
N2 - Purpose: Previous clinical observations suggested that coffee may have beneficial effects on the liver. In fact, an inverse relationship between coffee consumption and liver cirrhosis has been reported in humans. However, the causative role of coffee has not been established; therefore, the aim of this work was to study the effect of coffee in an experimental model of liver damage. Methods: In this work, cirrhosis was induced by chronic CCl4 administration and soluble or grain coffee (SC, GC, respectively) were co-administered for 8 weeks. Results: CCl4 administration elevated serum alkaline phosphatase and alanine aminotranspherase, liver lipid peroxidation, collagen content (fourfold) and TGF-β mRNA, and protein levels; depleted liver glycogen and reduced glutathione (GSH) content. Coffee prevented most of the changes produced by CCl4. Histopathological analysis was in agreement with biochemical and molecular data. The best effect was produced by GC. It is worth noting that GC preserved the normal collagen content as well as the normal TGF-β mRNA and protein levels. Conclusions: Our results suggest (1) that coffee plays a causative role in preventing cirrhosis (at least experimental cirrhosis); (2) that action mechanisms are probably associated with down regulation of the profibrogenic cytokine TGF-β and to its antioxidant properties and, (3) that GC is more potent than SC. These findings suggest a beneficial effect of coffee on the liver. However, more clinical and basic studies must be performed before reaching a final recommendation.
AB - Purpose: Previous clinical observations suggested that coffee may have beneficial effects on the liver. In fact, an inverse relationship between coffee consumption and liver cirrhosis has been reported in humans. However, the causative role of coffee has not been established; therefore, the aim of this work was to study the effect of coffee in an experimental model of liver damage. Methods: In this work, cirrhosis was induced by chronic CCl4 administration and soluble or grain coffee (SC, GC, respectively) were co-administered for 8 weeks. Results: CCl4 administration elevated serum alkaline phosphatase and alanine aminotranspherase, liver lipid peroxidation, collagen content (fourfold) and TGF-β mRNA, and protein levels; depleted liver glycogen and reduced glutathione (GSH) content. Coffee prevented most of the changes produced by CCl4. Histopathological analysis was in agreement with biochemical and molecular data. The best effect was produced by GC. It is worth noting that GC preserved the normal collagen content as well as the normal TGF-β mRNA and protein levels. Conclusions: Our results suggest (1) that coffee plays a causative role in preventing cirrhosis (at least experimental cirrhosis); (2) that action mechanisms are probably associated with down regulation of the profibrogenic cytokine TGF-β and to its antioxidant properties and, (3) that GC is more potent than SC. These findings suggest a beneficial effect of coffee on the liver. However, more clinical and basic studies must be performed before reaching a final recommendation.
KW - Antioxidants
KW - Carbon tetrachloride
KW - Cirrhosis
KW - Coffee
KW - Cytokines
KW - Fibrosis
KW - Liver damage
KW - TGF-β
UR - http://www.scopus.com/inward/record.url?scp=80055014268&partnerID=8YFLogxK
U2 - 10.1007/s12072-010-9247-6
DO - 10.1007/s12072-010-9247-6
M3 - Artículo
SN - 1936-0533
VL - 5
SP - 857
EP - 863
JO - Hepatology International
JF - Hepatology International
IS - 3
ER -