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Quyu Shengji Formula Facilitates Diabetic Wound Healing via Inhibiting the Expression of Prostaglandin Transporter
BACKGROUND: Quyu Shengji Formula (QSF), a Chinese medicine formula widely used in the clinic, has proven therapeutic effects on diabetic ulcers. Nevertheless, the potential mechanism of how QSF cures diabetic ulcer remains elusive. OBJECTIVE: To assess the mechanism of QSF against wound healing defe...
Autores principales: | , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7847361/ https://www.ncbi.nlm.nih.gov/pubmed/33552219 http://dx.doi.org/10.1155/2021/8849935 |
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author | Lu, Yi Ding, Xiaojie Qi, Fei Ru, Yi Kuai, Le Chen, Siting Yang, Yingyao Li, Xin Li, Fulun Li, Bin Zhou, Mi Ze, Kan |
author_facet | Lu, Yi Ding, Xiaojie Qi, Fei Ru, Yi Kuai, Le Chen, Siting Yang, Yingyao Li, Xin Li, Fulun Li, Bin Zhou, Mi Ze, Kan |
author_sort | Lu, Yi |
collection | PubMed |
description | BACKGROUND: Quyu Shengji Formula (QSF), a Chinese medicine formula widely used in the clinic, has proven therapeutic effects on diabetic ulcers. Nevertheless, the potential mechanism of how QSF cures diabetic ulcer remains elusive. OBJECTIVE: To assess the mechanism of QSF against wound healing defects in diabetes. METHODS: Db/db mice were adopted to determine the therapeutic potential of QSF. Further histology analysis was performed by hematoxylin and eosin (H&E) staining. Moreover, the expression patterns of prostaglandin transporter (PGT), prostaglandin E(2) (PGE(2)), and angiogenesis factor vascular endothelial growth factor (VEGF) were evaluated by immunostaining (IHC) analysis, ELISA assay, real-time quantitative polymerase chain reaction (RT-qPCR), and western blot analysis in vivo. Human dermal microvascular endothelial cells (HDMECs) and the shRNA interference technique were used to explore the effects of QSF on cell migration, PGT, PGE(2), and angiogenesis factor VEGF in vitro. RESULTS: Applied QSF on the wound of db/db mice significantly accelerated wound closure. Reductions of PGT and elevations of PGE(2) and increased angiogenesis factor VEGF levels were shown after QSF treatment in vivo and in vitro. Furthermore, QSF promoted HDMEC migration. Inhibition of the expression of PGT by shRNA reversed phenotypes of QSF treatment in vitro. CONCLUSION: Taken together, our findings reveal that QSF ameliorates diabetes-associated wound healing defects by abolishing the expression of PGT. |
format | Online Article Text |
id | pubmed-7847361 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Hindawi |
record_format | MEDLINE/PubMed |
spelling | pubmed-78473612021-02-04 Quyu Shengji Formula Facilitates Diabetic Wound Healing via Inhibiting the Expression of Prostaglandin Transporter Lu, Yi Ding, Xiaojie Qi, Fei Ru, Yi Kuai, Le Chen, Siting Yang, Yingyao Li, Xin Li, Fulun Li, Bin Zhou, Mi Ze, Kan Evid Based Complement Alternat Med Research Article BACKGROUND: Quyu Shengji Formula (QSF), a Chinese medicine formula widely used in the clinic, has proven therapeutic effects on diabetic ulcers. Nevertheless, the potential mechanism of how QSF cures diabetic ulcer remains elusive. OBJECTIVE: To assess the mechanism of QSF against wound healing defects in diabetes. METHODS: Db/db mice were adopted to determine the therapeutic potential of QSF. Further histology analysis was performed by hematoxylin and eosin (H&E) staining. Moreover, the expression patterns of prostaglandin transporter (PGT), prostaglandin E(2) (PGE(2)), and angiogenesis factor vascular endothelial growth factor (VEGF) were evaluated by immunostaining (IHC) analysis, ELISA assay, real-time quantitative polymerase chain reaction (RT-qPCR), and western blot analysis in vivo. Human dermal microvascular endothelial cells (HDMECs) and the shRNA interference technique were used to explore the effects of QSF on cell migration, PGT, PGE(2), and angiogenesis factor VEGF in vitro. RESULTS: Applied QSF on the wound of db/db mice significantly accelerated wound closure. Reductions of PGT and elevations of PGE(2) and increased angiogenesis factor VEGF levels were shown after QSF treatment in vivo and in vitro. Furthermore, QSF promoted HDMEC migration. Inhibition of the expression of PGT by shRNA reversed phenotypes of QSF treatment in vitro. CONCLUSION: Taken together, our findings reveal that QSF ameliorates diabetes-associated wound healing defects by abolishing the expression of PGT. Hindawi 2021-01-22 /pmc/articles/PMC7847361/ /pubmed/33552219 http://dx.doi.org/10.1155/2021/8849935 Text en Copyright © 2021 Yi Lu et al. https://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Lu, Yi Ding, Xiaojie Qi, Fei Ru, Yi Kuai, Le Chen, Siting Yang, Yingyao Li, Xin Li, Fulun Li, Bin Zhou, Mi Ze, Kan Quyu Shengji Formula Facilitates Diabetic Wound Healing via Inhibiting the Expression of Prostaglandin Transporter |
title | Quyu Shengji Formula Facilitates Diabetic Wound Healing via Inhibiting the Expression of Prostaglandin Transporter |
title_full | Quyu Shengji Formula Facilitates Diabetic Wound Healing via Inhibiting the Expression of Prostaglandin Transporter |
title_fullStr | Quyu Shengji Formula Facilitates Diabetic Wound Healing via Inhibiting the Expression of Prostaglandin Transporter |
title_full_unstemmed | Quyu Shengji Formula Facilitates Diabetic Wound Healing via Inhibiting the Expression of Prostaglandin Transporter |
title_short | Quyu Shengji Formula Facilitates Diabetic Wound Healing via Inhibiting the Expression of Prostaglandin Transporter |
title_sort | quyu shengji formula facilitates diabetic wound healing via inhibiting the expression of prostaglandin transporter |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7847361/ https://www.ncbi.nlm.nih.gov/pubmed/33552219 http://dx.doi.org/10.1155/2021/8849935 |
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