Background: Coffee is one of the most commonly consumed beverages worldwide. Accumulating clinical evidence has shown an inverse relationship between coffee and liver cirrhosis. We investigated the protective effect of coffee against liver fibrosis and underlying molecular mechanisms using a dimethylnitrosamine (DMN)-induced liver fibrosis model.
Results: Coffee administration significantly prevented the deterioration of body weight, organ weight, and serum biochemistry by DMN treatment. Histopathological examination revealed that necrosis/inflammation and fibrotic septa decreased significantly in coffee-treated rats compared to those treated with DMN and water. Coffee administration also significantly inhibited the accumulation of hydroxyproline (P < 0.001) and the production of malondialdehyde (P < 0.05), as well as stellate cell activation caused by DMN injection. Coffee protected the depletion of glutathione, superoxide dismutase, and catalase in liver tissue. In addition, coffee treatment inhibited the gene expression of inducible nitric oxide synthase, transforming growth factor (TGF)-beta, tumor necrosis factor-alpha, interleukin-1, and platelet-derived growth factor (PDGF)-beta in liver tissues, and lowered the concentration of TGF-beta and PDGF-beta in liver. Coffee inhibited NO production by macrophages.
Conclusion: Coffee exerts protective effects against liver fibrosis via antioxidant action and the suppression of fibrogenic cytokines, TGF-beta and PDGF-beta.