Abstract
Objectives: In various liver disease models, including those for alcoholic liver diseases, curcumin, a polyphenolic compound derived fromCurcuma longa, is known to have an hepatoprotective effect. However, the mechanism of action underlying its effects on alcohol-induced hepaticfibrosis remains unknown. We aimed to investigate the mechanisms of action underlying the effects of curcumin, mainly involving the transforminggrowth factor (TGF)-β/Smad pathway.Methods: Hepatic stellate cells (HSCs), LX2, were incubated with 50 mM ethanol with or without curcumin (1 and 10 μM). Viable HSCs were countedusing a LUNATM automated cell counter, whereas the expressions of TGF-β, Smad3, tissue inhibitor of metalloproteinases-1 (TIMP-1), and type 1collagen mRNA were measured using quantitative reverse transcriptase polymerase chain reactions.Results: Curcumin significantly suppressed ethanol-induced HSCs proliferation. The antiproliferative effect of curcumin appeared to be dosedependent. In addition, the mRNA expressions of TGF-β, Smad3, TIMP-1, and type 1 collagen decreased in the cells treated with curcumin.Conclusion: Curcumin seems to attenuate ethanol-induced HSCs proliferation through the suppression of TGF-β and appears to reduce the productionof extracellular matrix as shown by the decreased expression of type 1 collagen.
Highlights
Heavy alcohol consumption is a causal factor of multiorgan dysfunction, including alcoholic liver disease (ALD) [1]
We aimed to investigate the mechanism of action of curcumin on alcohol-induced hepatic fibrosis mainly through transforming growth factor (TGF)-β/Smad pathway
The increased cell viability was in accordance with the increase in TGF-β mRNA and Smad3 mRNA expressions
Summary
Heavy alcohol consumption is a causal factor of multiorgan dysfunction, including alcoholic liver disease (ALD) [1]. The clinical manifestations of ALD may vary depending on the disease stage, which can range from steatosis (fatty liver) to alcoholic hepatitis (fatty liver with inflammation). Liver fibrosis is an excessive accumulation of extracellular matrix (ECM) as a response to liver injuries. Hepatic stellate cells (HSCs) are known to play an important role in the development of liver fibrosis. HSCs remain inactive in the normal liver as retinoid storage cells and are activated during the processes leading to liver fibrosis. Activation of HSCs is characterized by increased cell proliferation, enhanced matrix production, and expression of a number of proliferative and profibrogenic cytokines and their receptors [5]
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