Coffee attenuates fibrosis by decreasing the expression of TGF‐β and CTGF in a murine model of liver damage

Abstract

This study was performed to evaluate the antifibrotic properties of coffee in a model of liver damage induced by repeated administration of thioacetamide (TAA) in male Wistar rats. In this study, cirrhosis was induced by chronic TAA administration and the effects of co-administration of conventional caffeinated coffee or decaffeinated coffee (CC, DC, respectively) for 8 weeks were evaluated. TAA administration elevated serum alkaline phosphatase (AP), γ-glutamyl transpeptidase (γ-GTP) and alanine aminotransferase (ALAT), liver lipid peroxidation, collagen content, depleted liver glycogen and glutathione peroxidase (GPx) activity. Additionally increased levels of a number of proteins were detected including transforming growth factor-beta (TGF-β), connective tissue growth factor (CTGF) and alpha-smooth muscle actin (α-SMA), and matrix metalloproteinase (MMP)-2, 9 and 13. Coffee suppressed most of the changes produced by TAA. Histopathological analysis was in agreement with biochemical and molecular findings. These results indicate that coffee attenuates experimental cirrhosis; the action mechanisms are probably associated with its antioxidant properties and mainly by its ability to block the elevation of the profibrogenic cytokine TGF-β and its downstream effector CTGF. Various components of coffee that have been related to such a favorable effect include caffeine, coffee oils kahweol, cafestol and antioxidant substances; however, no definite evidence for the role of these components has been established. These results support earlier findings suggesting a beneficial effect of coffee on the liver. However, more basic clinical studies must be performed to confirm this hypothesis.

Coffee as modulator of liver injury: Fact and fiction

“…12 An array of signaling factors are involved in activating HSCs including transforming growth factor-b (TGF-b) that promotes HSC differentiation and deposition of collagen, as well as inducing hepatocyte expression of connective tissue growth factor. 12,13 Multiple studies have shown an inhibitory effect of caffeine on TGF-b, 13 as well as a decreased expression of alpha-smooth muscle actin (a-SMA), a commonly used marker for the presence of activated HSCs. 14 These suggest that the overall effect of caffeine converges on decreasing the activation of HSCs, leading to decreased deposition of collagen and fibrosis ( Table 1).…”

A Mini Updated Review on the Role of Coffee in Non-Alcoholic Fatty Liver Disease

“…Coffee contains more than 1000 substances with the most important one, the chlorogenic acid (CGA) that has been found to decrease NAFLD development in rats by modulating glucose intolerance [6]. In addition, coffee has been found to reduce fibrosis in animal tissue by decreasing the expression of growth factor-b, which is responsible for the connective tissue growth factor that contributes to increase accumulation of fat in hepatic cells [7]. Furthermore, many studies have suggested the caffeine consumption plays a protective role in NAFLD [8][9][10].…”

Coffee Consumption to Reduce Liver Fibrosis

“…Coffee consists of various compound with good 4 Based on its concentration and physiological effect, there are three main components of coffee: 5 Caffeine Caffeine (1,3,7-trimethylxanthine) is a purin alkaloid with antagonist effect on adenosine subtype A 1 and A 2A receptor. Some physiological effect of caffeine are central nervous system stimulant, raise blood pressure, increase metabolic process, and diuretic.…”

“…In 8-weeks therapy, coffee consumption were proved to inhibit liver tissue damage caused by TAA. 5 Caffeine could prevent hepatic and its mRNA expression. Beside that, caffeine also reduce stellate hepatic cell activation by blocking caffeine were affect MMP 2 and 9 activity.…”