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Improvement Effect of Non-alcoholic Fatty Liver Disease by Curcuma longa L. Extract

강황 추출물의 비알코올성 지방간 질환 개선 효과

  • Lee, Young Seob (Department of Herbal Crop Research, NIHHS, RDA) ;
  • Lee, Dae Young (Department of Herbal Crop Research, NIHHS, RDA) ;
  • Kwon, Dong Yeul (Department of Oriental Pharmacy, College of Pharmacy, Wonkwang University) ;
  • Kang, Ok Hwa (Wonkwang Oriental Medicines Research Institute, Wonkwang University)
  • 이영섭 (농촌진흥청 국립원예특작과학원 인삼특작부 인삼특작이용팀) ;
  • 이대영 (농촌진흥청 국립원예특작과학원 인삼특작부 인삼특작이용팀) ;
  • 권동렬 (원광대학교 약학대학 한약학과) ;
  • 강옥화 (원광대학교 원광한약연구소)
  • Received : 2020.06.17
  • Accepted : 2020.07.29
  • Published : 2020.08.30

Abstract

Background: Non-alcoholic fatty liver disease (NAFLD) is a chronic liver disease associated with multiple metabolic disorders. The medicinal plant Curcuma longa L. is widely distributed in Asia and has been used to treat a spectrum diseases in clinical practice. To date, there are inadequate reports of the effects of C. longa 50% EtOH extract (CE) on NAFLD. Therefore, in this study, we evaluate the CE on an NAFLD animal and elucidate the mechanism of action. Methods and Results: C57BL/6J mice fed a methionine-choline deficient diet (MCD) were treated with CE or milk thistle, and changes in inflammation and stetosis were assessed. Experimental animals were divided into six group (n = 10); Normal, MCD, MCD + CE 50 mg/kg/day (CE 50), MCD + CE 100 mg/kg/day (CE 100), MCD + CE 150 mg/kg/day (CE 150), and the Control, MCD + Milk thistle 150 mg/kg/day (MT 150). Body weight, liver weight, liver function, and histological changes were assessed in experimental animals. Quantitative real-time polymerase chain reaction and western blot analyses were performed on samples collected after 4 weeks of treatment. We observed that CE administration improved MCD-diet-induced lipid accumulation, and triglyceride (TG) and total cholesterol (TC) levels in serum. Treatment with CE also decreased hepatic lipogenesis through modulation of the sterol regulatory element binding protein-1 (SREBP-1), CCAAT-enhancer binding protein α (C/EBPα), fatty acid synthase (FAS), and peroxisome proliferator-activated receptor γ (PPARγ) expresion. In addition, the use of CE increased adenosine monophosphate-activated protein kinase (AMPK) phosphorylation and inhibited the up-regulation of toll-like receptor (TLR)-2 and TLR-4 signaling and the production of inflammatory mediators. Conclusions: In this report, we observed that CE regulated lipid accumulation in an MCD dietinduced NAFLD model by decreasing lipogenesis. These data suggeste that CE could effectively protect mice against MCD-induced NAFLD, by inhibiting the TLR-2 and TLR-4 signaling cascades.

Keywords

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