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Spinosin ameliorates insulin resistance by suppressing reactive oxygen species-associated inflammation
OBJECTIVE(S): Spinosin is the predominant C-glycoside flavonoid derived from the seeds of Zizyphus jujuba var. Spinosa (Rhamnaceae). The present study aimed to investigate the effects of spinosin on insulin resistance (IR) in vascular endothelium. MATERIALS AND METHODS: The anti-IR effect of spinosi...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Mashhad University of Medical Sciences
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9392568/ https://www.ncbi.nlm.nih.gov/pubmed/36033948 http://dx.doi.org/10.22038/IJBMS.2022.64154.14127 |
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author | Ge, Chi-yu Yang, Ling Zhang, Jun-li Wei, Zhi-feng Feng, Feng |
author_facet | Ge, Chi-yu Yang, Ling Zhang, Jun-li Wei, Zhi-feng Feng, Feng |
author_sort | Ge, Chi-yu |
collection | PubMed |
description | OBJECTIVE(S): Spinosin is the predominant C-glycoside flavonoid derived from the seeds of Zizyphus jujuba var. Spinosa (Rhamnaceae). The present study aimed to investigate the effects of spinosin on insulin resistance (IR) in vascular endothelium. MATERIALS AND METHODS: The anti-IR effect of spinosin was evaluated in a high-fat diet (HFD) treated mice model. The effects of spinosin pretreatment on reactive oxygen species (ROS)-associated inflammation in Human umbilical vein endothelial cells (HUVEC) were evaluated by western blot analysis and reverse transcription-polymerase chain reaction. The effect of spinosin on insulin-mediated endothelium-dependent vasodilation of rat aortae was further evaluated. RESULTS: Spinosin at 20 mg/kg alleviates increased mice’s body weight, fasting serum glucose, oral glucose tolerance, serum insulin, insulin resistance index, and serum lipid of HFD-treated mice. Spinosin at 20 μM suppressed ROS overproduction, and inhibited ROS-related HUVEC inflammation by inhibiting mRNA expression of tumor necrosis factor-α and interleukin-6. In addition, spinosin at 0.1 μM showed a vasodilation effect of isoprenaline-pretreated rat aortae and increased insulin-mediated NO production in endothelial cells. These effects were shown to be related to the spinosin regulating serine/tyrosine phosphorylation of insulin receptor substrate-1 (IRS-1) facilitated/phosphoinositide 3-kinase (PI3K) signaling. CONCLUSION: Spinosin may ameliorate IR and ROS-associated inflammation, and increase endothelial NO production by mediating IRS-1/PI3K/endothelial nitric oxide synthase (eNOS) pathway. |
format | Online Article Text |
id | pubmed-9392568 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Mashhad University of Medical Sciences |
record_format | MEDLINE/PubMed |
spelling | pubmed-93925682022-08-26 Spinosin ameliorates insulin resistance by suppressing reactive oxygen species-associated inflammation Ge, Chi-yu Yang, Ling Zhang, Jun-li Wei, Zhi-feng Feng, Feng Iran J Basic Med Sci Original Article OBJECTIVE(S): Spinosin is the predominant C-glycoside flavonoid derived from the seeds of Zizyphus jujuba var. Spinosa (Rhamnaceae). The present study aimed to investigate the effects of spinosin on insulin resistance (IR) in vascular endothelium. MATERIALS AND METHODS: The anti-IR effect of spinosin was evaluated in a high-fat diet (HFD) treated mice model. The effects of spinosin pretreatment on reactive oxygen species (ROS)-associated inflammation in Human umbilical vein endothelial cells (HUVEC) were evaluated by western blot analysis and reverse transcription-polymerase chain reaction. The effect of spinosin on insulin-mediated endothelium-dependent vasodilation of rat aortae was further evaluated. RESULTS: Spinosin at 20 mg/kg alleviates increased mice’s body weight, fasting serum glucose, oral glucose tolerance, serum insulin, insulin resistance index, and serum lipid of HFD-treated mice. Spinosin at 20 μM suppressed ROS overproduction, and inhibited ROS-related HUVEC inflammation by inhibiting mRNA expression of tumor necrosis factor-α and interleukin-6. In addition, spinosin at 0.1 μM showed a vasodilation effect of isoprenaline-pretreated rat aortae and increased insulin-mediated NO production in endothelial cells. These effects were shown to be related to the spinosin regulating serine/tyrosine phosphorylation of insulin receptor substrate-1 (IRS-1) facilitated/phosphoinositide 3-kinase (PI3K) signaling. CONCLUSION: Spinosin may ameliorate IR and ROS-associated inflammation, and increase endothelial NO production by mediating IRS-1/PI3K/endothelial nitric oxide synthase (eNOS) pathway. Mashhad University of Medical Sciences 2022-07 /pmc/articles/PMC9392568/ /pubmed/36033948 http://dx.doi.org/10.22038/IJBMS.2022.64154.14127 Text en https://creativecommons.org/licenses/by/3.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution License, (http://creativecommons.org/licenses/by/3.0/ (https://creativecommons.org/licenses/by/3.0/) ) which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Article Ge, Chi-yu Yang, Ling Zhang, Jun-li Wei, Zhi-feng Feng, Feng Spinosin ameliorates insulin resistance by suppressing reactive oxygen species-associated inflammation |
title | Spinosin ameliorates insulin resistance by suppressing reactive oxygen species-associated inflammation |
title_full | Spinosin ameliorates insulin resistance by suppressing reactive oxygen species-associated inflammation |
title_fullStr | Spinosin ameliorates insulin resistance by suppressing reactive oxygen species-associated inflammation |
title_full_unstemmed | Spinosin ameliorates insulin resistance by suppressing reactive oxygen species-associated inflammation |
title_short | Spinosin ameliorates insulin resistance by suppressing reactive oxygen species-associated inflammation |
title_sort | spinosin ameliorates insulin resistance by suppressing reactive oxygen species-associated inflammation |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9392568/ https://www.ncbi.nlm.nih.gov/pubmed/36033948 http://dx.doi.org/10.22038/IJBMS.2022.64154.14127 |
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