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Hypolipidemic effect and molecular mechanism of ginsenosides: a review based on oxidative stress

Hyperlipidemia is considered a risk factor for cardiovascular and endocrine diseases. However, effective approaches for treating this common metabolic disorder remain limited. Ginseng has traditionally been used as a natural medicine for invigorating energy or “Qi” and has been demonstrated to posse...

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Autores principales: Jin, Wei, Li, Chunrun, Yang, Shihui, Song, Shiyi, Hou, Weiwei, Song, Yang, Du, Quanyu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10175615/
https://www.ncbi.nlm.nih.gov/pubmed/37188264
http://dx.doi.org/10.3389/fphar.2023.1166898
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author Jin, Wei
Li, Chunrun
Yang, Shihui
Song, Shiyi
Hou, Weiwei
Song, Yang
Du, Quanyu
author_facet Jin, Wei
Li, Chunrun
Yang, Shihui
Song, Shiyi
Hou, Weiwei
Song, Yang
Du, Quanyu
author_sort Jin, Wei
collection PubMed
description Hyperlipidemia is considered a risk factor for cardiovascular and endocrine diseases. However, effective approaches for treating this common metabolic disorder remain limited. Ginseng has traditionally been used as a natural medicine for invigorating energy or “Qi” and has been demonstrated to possess antioxidative, anti-apoptotic, and anti-inflammatory properties. A large number of studies have shown that ginsenosides, the main active ingredient of ginseng, have lipid-lowering effects. However, there remains a lack of systematic reviews detailing the molecular mechanisms by which ginsenosides reduce blood lipid levels, especially in relation to oxidative stress. For this article, research studies detailing the molecular mechanisms through which ginsenosides regulate oxidative stress and lower blood lipids in the treatment of hyperlipidemia and its related diseases (diabetes, nonalcoholic fatty liver disease, and atherosclerosis) were comprehensively reviewed. The relevant papers were search on seven literature databases. According to the studies reviewed, ginsenosides Rb1, Rb2, Rb3, Re, Rg1, Rg3, Rh2, Rh4, and F2 inhibit oxidative stress by increasing the activity of antioxidant enzymes, promoting fatty acid β-oxidation and autophagy, and regulating the intestinal flora to alleviate high blood pressure and improve the body’s lipid status. These effects are related to the regulation of various signaling pathways, such as those of PPARα, Nrf2, mitogen-activated protein kinases, SIRT3/FOXO3/SOD, and AMPK/SIRT1. These findings suggest that ginseng is a natural medicine with lipid-lowering effects.
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spelling pubmed-101756152023-05-13 Hypolipidemic effect and molecular mechanism of ginsenosides: a review based on oxidative stress Jin, Wei Li, Chunrun Yang, Shihui Song, Shiyi Hou, Weiwei Song, Yang Du, Quanyu Front Pharmacol Pharmacology Hyperlipidemia is considered a risk factor for cardiovascular and endocrine diseases. However, effective approaches for treating this common metabolic disorder remain limited. Ginseng has traditionally been used as a natural medicine for invigorating energy or “Qi” and has been demonstrated to possess antioxidative, anti-apoptotic, and anti-inflammatory properties. A large number of studies have shown that ginsenosides, the main active ingredient of ginseng, have lipid-lowering effects. However, there remains a lack of systematic reviews detailing the molecular mechanisms by which ginsenosides reduce blood lipid levels, especially in relation to oxidative stress. For this article, research studies detailing the molecular mechanisms through which ginsenosides regulate oxidative stress and lower blood lipids in the treatment of hyperlipidemia and its related diseases (diabetes, nonalcoholic fatty liver disease, and atherosclerosis) were comprehensively reviewed. The relevant papers were search on seven literature databases. According to the studies reviewed, ginsenosides Rb1, Rb2, Rb3, Re, Rg1, Rg3, Rh2, Rh4, and F2 inhibit oxidative stress by increasing the activity of antioxidant enzymes, promoting fatty acid β-oxidation and autophagy, and regulating the intestinal flora to alleviate high blood pressure and improve the body’s lipid status. These effects are related to the regulation of various signaling pathways, such as those of PPARα, Nrf2, mitogen-activated protein kinases, SIRT3/FOXO3/SOD, and AMPK/SIRT1. These findings suggest that ginseng is a natural medicine with lipid-lowering effects. Frontiers Media S.A. 2023-04-28 /pmc/articles/PMC10175615/ /pubmed/37188264 http://dx.doi.org/10.3389/fphar.2023.1166898 Text en Copyright © 2023 Jin, Li, Yang, Song, Hou, Song and Du. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Pharmacology
Jin, Wei
Li, Chunrun
Yang, Shihui
Song, Shiyi
Hou, Weiwei
Song, Yang
Du, Quanyu
Hypolipidemic effect and molecular mechanism of ginsenosides: a review based on oxidative stress
title Hypolipidemic effect and molecular mechanism of ginsenosides: a review based on oxidative stress
title_full Hypolipidemic effect and molecular mechanism of ginsenosides: a review based on oxidative stress
title_fullStr Hypolipidemic effect and molecular mechanism of ginsenosides: a review based on oxidative stress
title_full_unstemmed Hypolipidemic effect and molecular mechanism of ginsenosides: a review based on oxidative stress
title_short Hypolipidemic effect and molecular mechanism of ginsenosides: a review based on oxidative stress
title_sort hypolipidemic effect and molecular mechanism of ginsenosides: a review based on oxidative stress
topic Pharmacology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10175615/
https://www.ncbi.nlm.nih.gov/pubmed/37188264
http://dx.doi.org/10.3389/fphar.2023.1166898
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