THE EFFECT OF CURCUMIN ON THE PROLIFERATION AND EXTRACELLULAR MATRIX PRODUCTION IN ETHANOL-INDUCED HEPATIC STELLATE CELLS
Rahmaniah Rahmaniah, Melva Louisa, Bantari Wisynu Kusuma Wardhani, Vivian Soetikno
Abstract
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Rahmaniah Rahmaniah, Melva Louisa, Bantari Wisynu Kusuma Wardhani, Vivian Soetikno
Abstract
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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.
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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.
Key concepts: Curcumin, Hepatic stellate cell, Chemistry, Matrix metalloproteinase, Extracellular matrix, Ethanol, Transforming growth factor, Pharmacology