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논문 기본 정보

자료유형
학술저널
저자정보
이영섭 (농촌진흥청) 이대영 (농촌진흥청) 권동렬 (원광대학교) 강옥화 (원광대학교)
저널정보
한국약용작물학회 한국약용작물학회지 한국약용작물학회지 제28권 제4호
발행연도
2020.8
수록면
276 - 286 (11page)
DOI
10.7783/KJMCS.2020.28.4.276

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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 ㎎/㎏/day (CE 50), MCD + CE 100 ㎎/㎏/day (CE 100), MCD + CE 150 ㎎/㎏/day (CE 150), and the Control, MCD + Milk thistle 150 ㎎/㎏/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 diet-induced 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.

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UCI(KEPA) : I410-ECN-0101-2020-480-001160372