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Synergetic protective effect of berberine and ginsenoside Rb1 against tumor necrosis factor alpha−induced inflammation in adipocytes

Obesity significantly impacts living a normal life by increasing morbidity. Additionally, obesity has been shown to be closely associated with severe inflammation in adipocytes. It is widely reported that berberine (BBR) has an anti-inflammatory effect and can reduce glucose and lipid accumulation,...

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Autores principales: Cai, Zhixing, Chen, Yue
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Taylor & Francis 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8810088/
https://www.ncbi.nlm.nih.gov/pubmed/34699329
http://dx.doi.org/10.1080/21655979.2021.1996508
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author Cai, Zhixing
Chen, Yue
author_facet Cai, Zhixing
Chen, Yue
author_sort Cai, Zhixing
collection PubMed
description Obesity significantly impacts living a normal life by increasing morbidity. Additionally, obesity has been shown to be closely associated with severe inflammation in adipocytes. It is widely reported that berberine (BBR) has an anti-inflammatory effect and can reduce glucose and lipid accumulation, whereas ginsenoside Rb1 (Rb1) has been shown to have a significant inhibitory effect on insulin resistance and lipid peroxidation. In this study, we aimed to explore the synergetic effect of BBR and Rb1 on tumor necrosis factor alpha (TNF-α)-treated adipocytes and the mechanisms underlying it. We found that TNF-α reduced cell viability, facilitated the production of inflammatory factors, induced adipogenesis, activated the nuclear factor kappa B (NF-κB) pathway, and increased the expression of peroxisome proliferator-activated receptor gamma, CCAAT enhancer-binding protein alpha, and sterol regulatory element-binding protein-1 c in adipocytes. However, these effects were significantly alleviated by BBR or Rb1. Additionally, a synergetic effect was observed when BBR and Rb1 were used in combination. The effects of BBR in combination with Rb1 on cell proliferation, inflammation, adipogenesis, and the NF-κB pathway in TNF-α-treated adipocytes were significantly abolished by receptor activator of nuclear factor kappa-Β ligand, which is an activator of the NF-κB pathway. Collectively, the results revealed that BBR and Rb1 have a synergetic protective effect against TNF-α-induced inflammation in adipocytes. The mechanism underlying this synergetic effect was found to be inhibition of the NF-κB signaling pathway.
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spelling pubmed-88100882022-02-03 Synergetic protective effect of berberine and ginsenoside Rb1 against tumor necrosis factor alpha−induced inflammation in adipocytes Cai, Zhixing Chen, Yue Bioengineered Research Paper Obesity significantly impacts living a normal life by increasing morbidity. Additionally, obesity has been shown to be closely associated with severe inflammation in adipocytes. It is widely reported that berberine (BBR) has an anti-inflammatory effect and can reduce glucose and lipid accumulation, whereas ginsenoside Rb1 (Rb1) has been shown to have a significant inhibitory effect on insulin resistance and lipid peroxidation. In this study, we aimed to explore the synergetic effect of BBR and Rb1 on tumor necrosis factor alpha (TNF-α)-treated adipocytes and the mechanisms underlying it. We found that TNF-α reduced cell viability, facilitated the production of inflammatory factors, induced adipogenesis, activated the nuclear factor kappa B (NF-κB) pathway, and increased the expression of peroxisome proliferator-activated receptor gamma, CCAAT enhancer-binding protein alpha, and sterol regulatory element-binding protein-1 c in adipocytes. However, these effects were significantly alleviated by BBR or Rb1. Additionally, a synergetic effect was observed when BBR and Rb1 were used in combination. The effects of BBR in combination with Rb1 on cell proliferation, inflammation, adipogenesis, and the NF-κB pathway in TNF-α-treated adipocytes were significantly abolished by receptor activator of nuclear factor kappa-Β ligand, which is an activator of the NF-κB pathway. Collectively, the results revealed that BBR and Rb1 have a synergetic protective effect against TNF-α-induced inflammation in adipocytes. The mechanism underlying this synergetic effect was found to be inhibition of the NF-κB signaling pathway. Taylor & Francis 2021-12-04 /pmc/articles/PMC8810088/ /pubmed/34699329 http://dx.doi.org/10.1080/21655979.2021.1996508 Text en © 2021 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. https://creativecommons.org/licenses/by/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Paper
Cai, Zhixing
Chen, Yue
Synergetic protective effect of berberine and ginsenoside Rb1 against tumor necrosis factor alpha−induced inflammation in adipocytes
title Synergetic protective effect of berberine and ginsenoside Rb1 against tumor necrosis factor alpha−induced inflammation in adipocytes
title_full Synergetic protective effect of berberine and ginsenoside Rb1 against tumor necrosis factor alpha−induced inflammation in adipocytes
title_fullStr Synergetic protective effect of berberine and ginsenoside Rb1 against tumor necrosis factor alpha−induced inflammation in adipocytes
title_full_unstemmed Synergetic protective effect of berberine and ginsenoside Rb1 against tumor necrosis factor alpha−induced inflammation in adipocytes
title_short Synergetic protective effect of berberine and ginsenoside Rb1 against tumor necrosis factor alpha−induced inflammation in adipocytes
title_sort synergetic protective effect of berberine and ginsenoside rb1 against tumor necrosis factor alpha−induced inflammation in adipocytes
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8810088/
https://www.ncbi.nlm.nih.gov/pubmed/34699329
http://dx.doi.org/10.1080/21655979.2021.1996508
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