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Hepato-protective Effects of Daucus carota L. Root Ethanol Extract through Activation of AMPK in HepG2 Cells

HepG2 세포에서 AMPK 활성화를 통한 호나복(胡蘿蔔) 에탄올 추출물의 간 세포 보호 효과

  • Kim, Doyeon (College of Korean Medicine, Daegu Haany University) ;
  • Park, Sang Mi (College of Korean Medicine, Daegu Haany University) ;
  • Byun, Sung Hui (College of Korean Medicine, Daegu Haany University) ;
  • Park, Chung A (College of Korean Medicine, Daegu Haany University) ;
  • Cho, Il Je (College of Korean Medicine, Daegu Haany University) ;
  • Kim, Sang Chan (College of Korean Medicine, Daegu Haany University)
  • 김도연 (대구한의대학교 한의과대학) ;
  • 박상미 (대구한의대학교 한의과대학) ;
  • 변성희 (대구한의대학교 한의과대학) ;
  • 박정아 (대구한의대학교 한의과대학) ;
  • 조일제 (대구한의대학교 한의과대학) ;
  • 김상찬 (대구한의대학교 한의과대학)
  • Received : 2018.11.05
  • Accepted : 2018.11.22
  • Published : 2018.11.30

Abstract

Objectives : In Traditional Korean medicine, Daucus carota L. has been used for treating dyspepsia, diarrhea, dysentery and cough. Recent pharmacognosic evidence showed D. carota has anti-oxidant, anti-cancer, anti-fungal, and hypotensive effects. Present study investigated hepato-protective effect of D. carota ethanol extract (DCE) against oxidative stress in HepG2 cells. Methods : After HepG2 cells were pretreated with different concentrations of DCE, the cells were exposed to tert-butyl hydroperoxide (tBHP) for inducing oxidative stress. Cell viability, hydrogen peroxide production, glutathione concentration, and mitochondrial membrane potentials were measured to explore hepato-protective effect of DCE. Phosphorylation of AMP-activated protein kinase (AMPK) and effect of compound C on cell viability were determined to investigate the role of AMPK on DCE-mediated cytoprotection. Results : DCE significantly decreased the tBHP-mediated cytotoxicity in a concentration dependent manner and reduced the changes on apoptosis-related proteins by tBHP in HepG2 cells. In addition, DCE significantly prevented hydrogen peroxide production, glutathione depletion, and mitochondrial membrane impairment induced by tBHP. Treatment with DCE increased phosphorylation of AMPK, and the DCE-mediated cytoprotection was abolished by pretreatment with compound C. Conclusions : These results demonstrate that DCE can protect hepatocytes from oxidative stress through activation of AMPK.

Keywords

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Fig 1. DCE inhibited tBHP-induced apoptosis in HepG2 cells.

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Fig. 2. DCE prevented tBHP-induced oxidative stress.

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Fig. 3. DCE protected HepG2 cells from oxidative stress through AMPK activation.

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