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Ginsenoside Rb1 Facilitates Browning by Repressing Wnt/β-Catenin Signaling in 3T3-L1 Adipocytes
BACKGROUND: The discovery of browning in white adipose tissue has provided new ideas for treating obesity. Many studies have reported that ginsenoside Rb1 (G-Rb1) has activity against diabetes, inflammation, and obesity, but further investigation is needed on the effect and mechanism of G-Rb1 on bro...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
International Scientific Literature, Inc.
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7849207/ https://www.ncbi.nlm.nih.gov/pubmed/33503016 http://dx.doi.org/10.12659/MSM.928619 |
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author | Fan, Qingxin Xi, Pengjiao Tian, Derun Jia, Lianqun Cao, Yuan Zhan, Kaixuan Sun, Tianwei Zhang, Yinlong Wang, Qiming |
author_facet | Fan, Qingxin Xi, Pengjiao Tian, Derun Jia, Lianqun Cao, Yuan Zhan, Kaixuan Sun, Tianwei Zhang, Yinlong Wang, Qiming |
author_sort | Fan, Qingxin |
collection | PubMed |
description | BACKGROUND: The discovery of browning in white adipose tissue has provided new ideas for treating obesity. Many studies have reported that ginsenoside Rb1 (G-Rb1) has activity against diabetes, inflammation, and obesity, but further investigation is needed on the effect and mechanism of G-Rb1 on browning. MATERIAL/METHODS: We treated 3T3-L1 adipocytes with 0–200 μM G-Rb1, and 0.5 μM Compound 3f and 30 μM SKL2001 were used to activate Wnt/β-catenin signaling. Adipocyte activity was evaluated by Cell Counting Kit-8. Oil Red O staining was used to detect the lipid droplets. Quantitative real-time polymerase chain reaction was used to measure the expression of Cd-137, Cited-1, Txb-1, Prdm-16, and Ucp-1 mRNA. Western blotting was used to measure the expression of Ucp-1, pGSK-3β (Ser 9), GSK-3β, and β-catenin proteins. The expression of Ucp-1 was also detected with immunofluorescence. RESULTS: Adipocyte activity was not affected by 0–100 μM G-Rb1. However, G-Rb1 dose-dependently reduced the accumulation of lipid droplets; increased the expression of Cd-137, Cited-1, Txb-1, Prdm-16, and Ucp-1 mRNA; and increased the expression of Ucp-1, pGSK-3β (Ser 9), GSK- 3β, and β-catenin proteins. The accumulation of lipid droplets and the expression of Ucp-1 protein decreased as β-catenin increased. CONCLUSIONS: G-Rb1 at various concentrations (0–100 μM) promoted the browning of adipocytes in a dose-dependent manner. Further, we confirmed that activation of Wnt/β-catenin signaling could inhibit browning. Therefore, the browning promoted by G-Rb1 may be associated with the inhibition of Wnt/β-catenin signaling. |
format | Online Article Text |
id | pubmed-7849207 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | International Scientific Literature, Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-78492072021-02-03 Ginsenoside Rb1 Facilitates Browning by Repressing Wnt/β-Catenin Signaling in 3T3-L1 Adipocytes Fan, Qingxin Xi, Pengjiao Tian, Derun Jia, Lianqun Cao, Yuan Zhan, Kaixuan Sun, Tianwei Zhang, Yinlong Wang, Qiming Med Sci Monit Lab/In Vitro Research BACKGROUND: The discovery of browning in white adipose tissue has provided new ideas for treating obesity. Many studies have reported that ginsenoside Rb1 (G-Rb1) has activity against diabetes, inflammation, and obesity, but further investigation is needed on the effect and mechanism of G-Rb1 on browning. MATERIAL/METHODS: We treated 3T3-L1 adipocytes with 0–200 μM G-Rb1, and 0.5 μM Compound 3f and 30 μM SKL2001 were used to activate Wnt/β-catenin signaling. Adipocyte activity was evaluated by Cell Counting Kit-8. Oil Red O staining was used to detect the lipid droplets. Quantitative real-time polymerase chain reaction was used to measure the expression of Cd-137, Cited-1, Txb-1, Prdm-16, and Ucp-1 mRNA. Western blotting was used to measure the expression of Ucp-1, pGSK-3β (Ser 9), GSK-3β, and β-catenin proteins. The expression of Ucp-1 was also detected with immunofluorescence. RESULTS: Adipocyte activity was not affected by 0–100 μM G-Rb1. However, G-Rb1 dose-dependently reduced the accumulation of lipid droplets; increased the expression of Cd-137, Cited-1, Txb-1, Prdm-16, and Ucp-1 mRNA; and increased the expression of Ucp-1, pGSK-3β (Ser 9), GSK- 3β, and β-catenin proteins. The accumulation of lipid droplets and the expression of Ucp-1 protein decreased as β-catenin increased. CONCLUSIONS: G-Rb1 at various concentrations (0–100 μM) promoted the browning of adipocytes in a dose-dependent manner. Further, we confirmed that activation of Wnt/β-catenin signaling could inhibit browning. Therefore, the browning promoted by G-Rb1 may be associated with the inhibition of Wnt/β-catenin signaling. International Scientific Literature, Inc. 2021-01-27 /pmc/articles/PMC7849207/ /pubmed/33503016 http://dx.doi.org/10.12659/MSM.928619 Text en © Med Sci Monit, 2021 This work is licensed under Creative Common Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0 (https://creativecommons.org/licenses/by-nc-nd/4.0/) ) |
spellingShingle | Lab/In Vitro Research Fan, Qingxin Xi, Pengjiao Tian, Derun Jia, Lianqun Cao, Yuan Zhan, Kaixuan Sun, Tianwei Zhang, Yinlong Wang, Qiming Ginsenoside Rb1 Facilitates Browning by Repressing Wnt/β-Catenin Signaling in 3T3-L1 Adipocytes |
title | Ginsenoside Rb1 Facilitates Browning by Repressing Wnt/β-Catenin Signaling in 3T3-L1 Adipocytes |
title_full | Ginsenoside Rb1 Facilitates Browning by Repressing Wnt/β-Catenin Signaling in 3T3-L1 Adipocytes |
title_fullStr | Ginsenoside Rb1 Facilitates Browning by Repressing Wnt/β-Catenin Signaling in 3T3-L1 Adipocytes |
title_full_unstemmed | Ginsenoside Rb1 Facilitates Browning by Repressing Wnt/β-Catenin Signaling in 3T3-L1 Adipocytes |
title_short | Ginsenoside Rb1 Facilitates Browning by Repressing Wnt/β-Catenin Signaling in 3T3-L1 Adipocytes |
title_sort | ginsenoside rb1 facilitates browning by repressing wnt/β-catenin signaling in 3t3-l1 adipocytes |
topic | Lab/In Vitro Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7849207/ https://www.ncbi.nlm.nih.gov/pubmed/33503016 http://dx.doi.org/10.12659/MSM.928619 |
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