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How Does Ginsenoside Rh2 Mitigate Adipogenesis in Cultured Cells and Obese Mice?

Ginsenoside Rh2, an intermediate metabolite of ginseng, but not naturally occurring, has recently drawn attention because of its anticancer effect. However, it is not clear if and how Rh2 inhibits preadipocytes differentiation. In the present study, we hypothesized that ginsenoside Rh2 attenuates ad...

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Autores principales: Zhang, Longyun, Virgous, Carlos, Si, Hongwei
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7287807/
https://www.ncbi.nlm.nih.gov/pubmed/32455850
http://dx.doi.org/10.3390/molecules25102412
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author Zhang, Longyun
Virgous, Carlos
Si, Hongwei
author_facet Zhang, Longyun
Virgous, Carlos
Si, Hongwei
author_sort Zhang, Longyun
collection PubMed
description Ginsenoside Rh2, an intermediate metabolite of ginseng, but not naturally occurring, has recently drawn attention because of its anticancer effect. However, it is not clear if and how Rh2 inhibits preadipocytes differentiation. In the present study, we hypothesized that ginsenoside Rh2 attenuates adipogenesis through regulating the peroxisome proliferator-activated receptor gamma (PPAR-γ) pathway both in cells and obese mice. Different concentrations of Rh2 were applied both in 3T3-L1 cells and human primary preadipocytes to determine if Rh2 inhibits cell differentiation. Dietary Rh2 was administered to obese mice to determine if Rh2 prevents obesity in vivo. The mRNA and protein expression of PPAR-γ pathway molecules in cells and tissues were measured by real-time polymerase chain reaction (RT-PCR) and Western blot, respectively. Our results show that Rh2 dose-dependently (30–60 μM) inhibited cell differentiation in 3T3-L1 cells (44.5% ± 7.8% of control at 60 μM). This inhibitory effect is accompanied by the attenuation of the protein and/or mRNA expression of adipogenic markers including PPAR-γ and CCAAT/enhancer binding protein alpha, fatty acid synthase, fatty acid binding protein 4, and perilipin significantly (p < 0.05). Moreover, Rh2 significantly (p < 0.05) inhibited differentiation in human primary preadipocytes at much lower concentrations (5–15 μM). Furthermore, dietary intake of Rh2 (0.1 g Rh2/kg diet, w/w for eight weeks) significantly (p < 0.05) reduced protein PPAR-γ expression in liver and hepatic glutathione reductase and lowered fasting blood glucose. These results suggest that ginsenoside Rh2 dose-dependently inhibits adipogenesis through down-regulating the PPAR-γ pathway, and Rh2 may be a potential agent in preventing obesity in vivo.
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spelling pubmed-72878072020-06-15 How Does Ginsenoside Rh2 Mitigate Adipogenesis in Cultured Cells and Obese Mice? Zhang, Longyun Virgous, Carlos Si, Hongwei Molecules Article Ginsenoside Rh2, an intermediate metabolite of ginseng, but not naturally occurring, has recently drawn attention because of its anticancer effect. However, it is not clear if and how Rh2 inhibits preadipocytes differentiation. In the present study, we hypothesized that ginsenoside Rh2 attenuates adipogenesis through regulating the peroxisome proliferator-activated receptor gamma (PPAR-γ) pathway both in cells and obese mice. Different concentrations of Rh2 were applied both in 3T3-L1 cells and human primary preadipocytes to determine if Rh2 inhibits cell differentiation. Dietary Rh2 was administered to obese mice to determine if Rh2 prevents obesity in vivo. The mRNA and protein expression of PPAR-γ pathway molecules in cells and tissues were measured by real-time polymerase chain reaction (RT-PCR) and Western blot, respectively. Our results show that Rh2 dose-dependently (30–60 μM) inhibited cell differentiation in 3T3-L1 cells (44.5% ± 7.8% of control at 60 μM). This inhibitory effect is accompanied by the attenuation of the protein and/or mRNA expression of adipogenic markers including PPAR-γ and CCAAT/enhancer binding protein alpha, fatty acid synthase, fatty acid binding protein 4, and perilipin significantly (p < 0.05). Moreover, Rh2 significantly (p < 0.05) inhibited differentiation in human primary preadipocytes at much lower concentrations (5–15 μM). Furthermore, dietary intake of Rh2 (0.1 g Rh2/kg diet, w/w for eight weeks) significantly (p < 0.05) reduced protein PPAR-γ expression in liver and hepatic glutathione reductase and lowered fasting blood glucose. These results suggest that ginsenoside Rh2 dose-dependently inhibits adipogenesis through down-regulating the PPAR-γ pathway, and Rh2 may be a potential agent in preventing obesity in vivo. MDPI 2020-05-21 /pmc/articles/PMC7287807/ /pubmed/32455850 http://dx.doi.org/10.3390/molecules25102412 Text en © 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Zhang, Longyun
Virgous, Carlos
Si, Hongwei
How Does Ginsenoside Rh2 Mitigate Adipogenesis in Cultured Cells and Obese Mice?
title How Does Ginsenoside Rh2 Mitigate Adipogenesis in Cultured Cells and Obese Mice?
title_full How Does Ginsenoside Rh2 Mitigate Adipogenesis in Cultured Cells and Obese Mice?
title_fullStr How Does Ginsenoside Rh2 Mitigate Adipogenesis in Cultured Cells and Obese Mice?
title_full_unstemmed How Does Ginsenoside Rh2 Mitigate Adipogenesis in Cultured Cells and Obese Mice?
title_short How Does Ginsenoside Rh2 Mitigate Adipogenesis in Cultured Cells and Obese Mice?
title_sort how does ginsenoside rh2 mitigate adipogenesis in cultured cells and obese mice?
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7287807/
https://www.ncbi.nlm.nih.gov/pubmed/32455850
http://dx.doi.org/10.3390/molecules25102412
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