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Effect of Baicalin on Wound Healing in a Mouse Model of Pressure Ulcers
One of the most frequent comorbidities that develop in chronically ill or immobilized patients is pressure ulcers, also known as bed sores. Despite ischemia-reperfusion (I/R)-induced skin lesion having been identified as a primary cause of pressure ulcers, wound management efforts have so far failed...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9820804/ https://www.ncbi.nlm.nih.gov/pubmed/36613772 http://dx.doi.org/10.3390/ijms24010329 |
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author | Kim, Eunbin Ham, Seoyoon Jung, Bok Ki Park, Jin-Woo Kim, Jihee Lee, Ju Hee |
author_facet | Kim, Eunbin Ham, Seoyoon Jung, Bok Ki Park, Jin-Woo Kim, Jihee Lee, Ju Hee |
author_sort | Kim, Eunbin |
collection | PubMed |
description | One of the most frequent comorbidities that develop in chronically ill or immobilized patients is pressure ulcers, also known as bed sores. Despite ischemia-reperfusion (I/R)-induced skin lesion having been identified as a primary cause of pressure ulcers, wound management efforts have so far failed to significantly improve outcomes. Baicalin, or 5,6,7-trihydroxyflavone, is a type of flavonoid which has been shown to possess a variety of biological characteristics, including antioxidative and anti-inflammatory effects and protection of I/R injury. In vitro wound scratch assay was first used to assess the function of baicalin in wound healing. We established a mouse model of advanced stage pressure ulcers with repeated cycles of I/R pressure load. In this model, topically applied baicalin (100 mg/mL) induced a significant increase in the wound healing process measured by wound area. Histological examination of the pressure ulcer mouse model showed faster granulation tissue formation and re-epithelization in the baicalin-treated group. Next, baicalin downregulated pro-inflammatory cytokines (IL-6 and IL-1β), while upregulating the anti-inflammatory IL-10. Additionally, baicalin induced an increase in several growth factors (VEGF, FGF-2, PDGF-β, and CTGF), promoting the wound healing process. Our results suggest that baicalin could serve as a promising agent for the treatment of pressures ulcers. |
format | Online Article Text |
id | pubmed-9820804 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-98208042023-01-07 Effect of Baicalin on Wound Healing in a Mouse Model of Pressure Ulcers Kim, Eunbin Ham, Seoyoon Jung, Bok Ki Park, Jin-Woo Kim, Jihee Lee, Ju Hee Int J Mol Sci Article One of the most frequent comorbidities that develop in chronically ill or immobilized patients is pressure ulcers, also known as bed sores. Despite ischemia-reperfusion (I/R)-induced skin lesion having been identified as a primary cause of pressure ulcers, wound management efforts have so far failed to significantly improve outcomes. Baicalin, or 5,6,7-trihydroxyflavone, is a type of flavonoid which has been shown to possess a variety of biological characteristics, including antioxidative and anti-inflammatory effects and protection of I/R injury. In vitro wound scratch assay was first used to assess the function of baicalin in wound healing. We established a mouse model of advanced stage pressure ulcers with repeated cycles of I/R pressure load. In this model, topically applied baicalin (100 mg/mL) induced a significant increase in the wound healing process measured by wound area. Histological examination of the pressure ulcer mouse model showed faster granulation tissue formation and re-epithelization in the baicalin-treated group. Next, baicalin downregulated pro-inflammatory cytokines (IL-6 and IL-1β), while upregulating the anti-inflammatory IL-10. Additionally, baicalin induced an increase in several growth factors (VEGF, FGF-2, PDGF-β, and CTGF), promoting the wound healing process. Our results suggest that baicalin could serve as a promising agent for the treatment of pressures ulcers. MDPI 2022-12-25 /pmc/articles/PMC9820804/ /pubmed/36613772 http://dx.doi.org/10.3390/ijms24010329 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/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 (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Kim, Eunbin Ham, Seoyoon Jung, Bok Ki Park, Jin-Woo Kim, Jihee Lee, Ju Hee Effect of Baicalin on Wound Healing in a Mouse Model of Pressure Ulcers |
title | Effect of Baicalin on Wound Healing in a Mouse Model of Pressure Ulcers |
title_full | Effect of Baicalin on Wound Healing in a Mouse Model of Pressure Ulcers |
title_fullStr | Effect of Baicalin on Wound Healing in a Mouse Model of Pressure Ulcers |
title_full_unstemmed | Effect of Baicalin on Wound Healing in a Mouse Model of Pressure Ulcers |
title_short | Effect of Baicalin on Wound Healing in a Mouse Model of Pressure Ulcers |
title_sort | effect of baicalin on wound healing in a mouse model of pressure ulcers |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9820804/ https://www.ncbi.nlm.nih.gov/pubmed/36613772 http://dx.doi.org/10.3390/ijms24010329 |
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