• Herbal Formula Science
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• v.26 no.3
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• pp.183-193
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• 2018

Objectives : In Traditional Korean Medicine, Epimedium koreanum Nakai has diverse pharmacological activities to treat impotence, forgetfulness, cataract and exophthalmos. Present study investigated anti-fibrogenic effects of E. koreanum water extract (EKE) in hepatic stellate cells (HSCs). Methods : To study anti-fibrogenic effects of EKE, LX-2 cells, a human immortalized HSCs, were pre-treated with $3-300{\mu}g/mL$ of EKE, and then subsequently exposed to 5 ng/mL of transforming growth $factor-{\beta}1$ ($TGF-{\beta}1$). Expression level of ${\alpha}-smooth$ muscle actin was determined by immunoblot analysis. Phosphorylation of Smad, transactivation of Smad, and expression of plasminogen activator inhibitor-1 (PAI-1) were monitored to investigate the effect of EKE on $TGF-{\beta}1-mediated$ signaling pathway. Results : Up to $100{\mu}g/mL$, EKE did not show any cytotoxicity on LX-2 cells. Pre-treatment of EKE ($100{\mu}g/mL$) significantly inhibited ${\alpha}-smooth$ muscle actin expression induced by $TGF-{\beta}1$. In addition, EKE significantly decreased Smad2 and Smad3 phosphorylations, Smad binding element-driven luciferase activity and PAI-1 expression by $TGF-{\beta}1$. Of three flavonoid compounds found in EKE, only quercertin ($30{\mu}M$) attenuated $TGF-{\beta}1-mediated$ PAI-1 expression. Conclusion : These results suggest that EKE has an ability to suppress fibrogenic process in HSCs via inhibition of $TGF-{\beta}1/Smad$ signaling pathway.

• Herbal Formula Science
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• v.32 no.1
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• pp.63-82
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• 2024

Objective : Saengkankunbi-tang (SKT) is used as a traditional Korean herbal formula for treatment of liver diseases. We investigated the hepatoprotective effects of SKT plus Epimedium koreanum Nakai (EKE) against arachidonic acid (AA) + iron-mediated cytotoxicity in HepG2 cells and carbon tetrachloride (CCl₄)-mediated acute liver damage in mice. Methods : The cyto-protective effects of SKT + EKE were determined by MTT assay, western blot and fluorescence activated cell sorting analysis. In mice, blood biochemistry and western blot were assessed in CCl₄-induced acute hepatic damage. The animal groups included vehicle-treated control, CCl₄, SKT (200 mg/kg/day), EKE (100 mg/kg/day), SKT (200 mg/kg/day) + EKE (100 mg/kg/day) and silymarin (200 mg/kg/day). Results : In HepG2 cells, pretreatment with SKT + EKE significantly suppressed cytotoxicity induced by AA + iron and reduced the expression of proteins related to apoptosis. In addition, pretreatment with SKT + EKE significantly prevented the increase in H₂O₂ production, GSH depletion, and lower mitochondrial membrane potential induced by AA + iron. In CCl₄-induced liver damage mice, the administration of SKT + EKE prevented the liver damage by inhibition of hepatocyte damage and expression of apoptosis proteins in liver. More importantly, in vitro and in vivo assay, SKT + EKE showed significant effect compare with SKT alone or EKE alone in all parameters. Conclusions : These results indicated that SKT + EKE could protect against oxidative stress-induced liver damage, and SKT + EKE is more effective than SKT alone or EKE alone.