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Caffeine attenuates liver fibrosis via defective adhesion of hepatic stellate cells in cirrhotic model
Author(s) -
Shim Sung Gon,
Jun Dae Won,
Kim Eun Kyung,
Saeed Waqar Khalid,
Lee Kang Nyeong,
Lee Hang Lak,
Lee Oh Young,
Choi Ho Soon,
Yoon Byung Chul
Publication year - 2013
Publication title -
journal of gastroenterology and hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.214
H-Index - 130
eISSN - 1440-1746
pISSN - 0815-9319
DOI - 10.1111/jgh.12317
Subject(s) - caffeine , hepatic stellate cell , medicine , fibrosis , cirrhosis , endocrinology , thioacetamide , hepatic fibrosis , inflammation
Abstract Background and Aim Several epidemiological studies have shown that coffee intake attenuates the progression of liver fibrosis; however, the mechanism is unclear. Aims We investigated the direct effects of caffeine on hepatic stellate cells ( HSC s) and assessed whether caffeine attenuated intrahepatic fibrosis in rat model of liver cirrhosis. Methods Human hepatic stellate cell line, an immortalized human HSC s line, was used in in vitro assay system. Cell migration and proliferation were assessed in presence of various caffeine concentrations (0, 1, 5, and 10 mmol), and levels of procollagen type I c and α‐smooth muscle actin (α‐SMA) were measured by W estern blot. Severity of liver inflammation and fibrosis were compared between thioacetamide‐treated rats with and without caffeine supplementation. Results Caffeine increased HSC s apoptosis and intracellular F ‐actin and cyclic adenosine monophosphate expression. Caffeine also inhibited procollagen type I c and α‐ SMA expression in a dose‐ and time‐dependent manner. In rat model, caffeine decreased periportal inflammation, levels of inflammatory cells (1.4 ± 0.52 vs 2.6 ± 0.46, P < 0.05), and fibrosis (2.1 ± 0.35 vs 2.9 ± 0.84, P < 0.05). Transforming growth factor‐β and α‐ SMA expressions were also reduced by caffeine. Conclusion Caffeine attenuates the progression of liver fibrosis by inhibiting HSC s adhesion and activation.