Mogroside V Protects against Hepatic Steatosis in Mice on a High-Fat Diet and LO2 Cells Treated with Free Fatty Acids via AMPK Activation

Previous studies presented various beneficial effects of mogrosides extract from Siraitia grosvenorii, which has been included in the list of Medicine Food Homology Species in China. Mogroside V (MV) is one of the main ingredients in mogrosides extract; however, whether and how MV improves impaired...

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Main Authors: Linghuan Li, Wanfang Zheng, Can Wang, Jiameng Qi, Hanbing Li
Format: Article
Language:English
Published: Hindawi Limited 2020-01-01
Series:Evidence-Based Complementary and Alternative Medicine
Online Access:http://dx.doi.org/10.1155/2020/7826874
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spelling doaj-07c0185f28cb476da77e55cdefb1c65c2020-11-25T02:58:54ZengHindawi LimitedEvidence-Based Complementary and Alternative Medicine1741-427X1741-42882020-01-01202010.1155/2020/78268747826874Mogroside V Protects against Hepatic Steatosis in Mice on a High-Fat Diet and LO2 Cells Treated with Free Fatty Acids via AMPK ActivationLinghuan Li0Wanfang Zheng1Can Wang2Jiameng Qi3Hanbing Li4Institute of Pharmacology, Zhejiang University of Technology, Hangzhou 310014, ChinaInstitute of Pharmacology, Zhejiang University of Technology, Hangzhou 310014, ChinaInstitute of Pharmacology, Zhejiang University of Technology, Hangzhou 310014, ChinaInstitute of Pharmacology, Zhejiang University of Technology, Hangzhou 310014, ChinaInstitute of Pharmacology, Zhejiang University of Technology, Hangzhou 310014, ChinaPrevious studies presented various beneficial effects of mogrosides extract from Siraitia grosvenorii, which has been included in the list of Medicine Food Homology Species in China. Mogroside V (MV) is one of the main ingredients in mogrosides extract; however, whether and how MV improves impaired lipid metabolism in the liver remains to be elucidated. Herein, we investigated the therapeutic effects of mogroside V upon hepatic steatosis in vivo and in vitro and explored the underlying mechanisms. The results showed that MV significantly ameliorated hepatic steatosis in high-fat diet- (HFD-) fed mice. Furthermore, the increased protein expression of PPAR-γ, SREBP-1, and FASN and mRNA expression of pparg, srebp1, scd1, and fasn in the liver in HFD-fed mice, which contribute to de novo lipogenesis, were dose-dependently reversed by MV treatment. Meanwhile, MV counteracted the suppressed expression of PPAR-α and CPT-1A and mRNA expression of atgl, hsl, ppara, and cpt1a, thus increasing lipolysis and fatty acid oxidation. In addition, in free fatty acids- (FFAs-) incubated LO2 cells MV downregulated de novo lipogenesis and upregulated lipolysis and fatty acid oxidation, thereby attenuating lipid accumulation, which was significantly abrogated by treatment with Compound C, an inhibitor of AMP-activated protein kinase (AMPK). Taken together, these results suggested that MV exerted a pronounced effect upon improving hepatic steatosis through regulating the disequilibrium of lipid metabolism in the liver via an AMPK-dependent pathway, providing a potential lead compound candidate for preventing nonalcoholic fatty liver disease.http://dx.doi.org/10.1155/2020/7826874
collection DOAJ
language English
format Article
sources DOAJ
author Linghuan Li
Wanfang Zheng
Can Wang
Jiameng Qi
Hanbing Li
spellingShingle Linghuan Li
Wanfang Zheng
Can Wang
Jiameng Qi
Hanbing Li
Mogroside V Protects against Hepatic Steatosis in Mice on a High-Fat Diet and LO2 Cells Treated with Free Fatty Acids via AMPK Activation
Evidence-Based Complementary and Alternative Medicine
author_facet Linghuan Li
Wanfang Zheng
Can Wang
Jiameng Qi
Hanbing Li
author_sort Linghuan Li
title Mogroside V Protects against Hepatic Steatosis in Mice on a High-Fat Diet and LO2 Cells Treated with Free Fatty Acids via AMPK Activation
title_short Mogroside V Protects against Hepatic Steatosis in Mice on a High-Fat Diet and LO2 Cells Treated with Free Fatty Acids via AMPK Activation
title_full Mogroside V Protects against Hepatic Steatosis in Mice on a High-Fat Diet and LO2 Cells Treated with Free Fatty Acids via AMPK Activation
title_fullStr Mogroside V Protects against Hepatic Steatosis in Mice on a High-Fat Diet and LO2 Cells Treated with Free Fatty Acids via AMPK Activation
title_full_unstemmed Mogroside V Protects against Hepatic Steatosis in Mice on a High-Fat Diet and LO2 Cells Treated with Free Fatty Acids via AMPK Activation
title_sort mogroside v protects against hepatic steatosis in mice on a high-fat diet and lo2 cells treated with free fatty acids via ampk activation
publisher Hindawi Limited
series Evidence-Based Complementary and Alternative Medicine
issn 1741-427X
1741-4288
publishDate 2020-01-01
description Previous studies presented various beneficial effects of mogrosides extract from Siraitia grosvenorii, which has been included in the list of Medicine Food Homology Species in China. Mogroside V (MV) is one of the main ingredients in mogrosides extract; however, whether and how MV improves impaired lipid metabolism in the liver remains to be elucidated. Herein, we investigated the therapeutic effects of mogroside V upon hepatic steatosis in vivo and in vitro and explored the underlying mechanisms. The results showed that MV significantly ameliorated hepatic steatosis in high-fat diet- (HFD-) fed mice. Furthermore, the increased protein expression of PPAR-γ, SREBP-1, and FASN and mRNA expression of pparg, srebp1, scd1, and fasn in the liver in HFD-fed mice, which contribute to de novo lipogenesis, were dose-dependently reversed by MV treatment. Meanwhile, MV counteracted the suppressed expression of PPAR-α and CPT-1A and mRNA expression of atgl, hsl, ppara, and cpt1a, thus increasing lipolysis and fatty acid oxidation. In addition, in free fatty acids- (FFAs-) incubated LO2 cells MV downregulated de novo lipogenesis and upregulated lipolysis and fatty acid oxidation, thereby attenuating lipid accumulation, which was significantly abrogated by treatment with Compound C, an inhibitor of AMP-activated protein kinase (AMPK). Taken together, these results suggested that MV exerted a pronounced effect upon improving hepatic steatosis through regulating the disequilibrium of lipid metabolism in the liver via an AMPK-dependent pathway, providing a potential lead compound candidate for preventing nonalcoholic fatty liver disease.
url http://dx.doi.org/10.1155/2020/7826874
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