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Notoginseng Triterpenes Inhibited Autophagy in Random Flaps via the Beclin-1/VPS34/LC3 Signaling Pathway to Improve Tissue Survival
Random flaps are widely used in tissue reconstruction, attributed to the lack of vascular axial limitation. Nevertheless, the distal end of the flap is prone to necrosis due to the lack of blood supply. Notoginseng triterpenes (NTs) are the active components extracted from Panax notoginseng, reducin...
Autores principales: | , , , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Frontiers Media S.A.
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8640242/ https://www.ncbi.nlm.nih.gov/pubmed/34869285 http://dx.doi.org/10.3389/fbioe.2021.771066 |
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author | Huang, Zhiyang Luo, Xiaobin Zhang, Yifan Ying, Yibo Cai, Xiong Lu, Wenjie Zhao, Juan Wang, Yutian Lin, Wenwei Tu, Yurong Xiang, Ziyue Wu, Qiuji Yang, Shengwu Zhu, Sipin Li, Xiaoyang |
author_facet | Huang, Zhiyang Luo, Xiaobin Zhang, Yifan Ying, Yibo Cai, Xiong Lu, Wenjie Zhao, Juan Wang, Yutian Lin, Wenwei Tu, Yurong Xiang, Ziyue Wu, Qiuji Yang, Shengwu Zhu, Sipin Li, Xiaoyang |
author_sort | Huang, Zhiyang |
collection | PubMed |
description | Random flaps are widely used in tissue reconstruction, attributed to the lack of vascular axial limitation. Nevertheless, the distal end of the flap is prone to necrosis due to the lack of blood supply. Notoginseng triterpenes (NTs) are the active components extracted from Panax notoginseng, reducing oxygen consumption and improving the body’s tolerance to hypoxia. However, their role in random flap survival has not been elucidated. In this study, we used a mouse random skin flap model to verify that NT can promote cell proliferation and migration and that increasing blood perfusion can effectively improve the survival area of a skin flap. Our study also showed that the autophagy of random flaps after NT treatment was activated through the Beclin-1/VPS34/LC3 signaling pathway, and the therapeutic effect of NT significantly decreased after VPS34 IN inhibited autophagy. In conclusion, we have demonstrated that NT can significantly improve the survival rate of random flaps through the Beclin-1/VPS34/LC3 signaling pathway, suggesting that it might be a promising clinical treatment option. |
format | Online Article Text |
id | pubmed-8640242 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-86402422021-12-04 Notoginseng Triterpenes Inhibited Autophagy in Random Flaps via the Beclin-1/VPS34/LC3 Signaling Pathway to Improve Tissue Survival Huang, Zhiyang Luo, Xiaobin Zhang, Yifan Ying, Yibo Cai, Xiong Lu, Wenjie Zhao, Juan Wang, Yutian Lin, Wenwei Tu, Yurong Xiang, Ziyue Wu, Qiuji Yang, Shengwu Zhu, Sipin Li, Xiaoyang Front Bioeng Biotechnol Bioengineering and Biotechnology Random flaps are widely used in tissue reconstruction, attributed to the lack of vascular axial limitation. Nevertheless, the distal end of the flap is prone to necrosis due to the lack of blood supply. Notoginseng triterpenes (NTs) are the active components extracted from Panax notoginseng, reducing oxygen consumption and improving the body’s tolerance to hypoxia. However, their role in random flap survival has not been elucidated. In this study, we used a mouse random skin flap model to verify that NT can promote cell proliferation and migration and that increasing blood perfusion can effectively improve the survival area of a skin flap. Our study also showed that the autophagy of random flaps after NT treatment was activated through the Beclin-1/VPS34/LC3 signaling pathway, and the therapeutic effect of NT significantly decreased after VPS34 IN inhibited autophagy. In conclusion, we have demonstrated that NT can significantly improve the survival rate of random flaps through the Beclin-1/VPS34/LC3 signaling pathway, suggesting that it might be a promising clinical treatment option. Frontiers Media S.A. 2021-11-19 /pmc/articles/PMC8640242/ /pubmed/34869285 http://dx.doi.org/10.3389/fbioe.2021.771066 Text en Copyright © 2021 Huang, Luo, Zhang, Ying, Cai, Lu, Zhao, Wang, Lin, Tu, Xiang, Wu, Yang, Zhu and Li. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Bioengineering and Biotechnology Huang, Zhiyang Luo, Xiaobin Zhang, Yifan Ying, Yibo Cai, Xiong Lu, Wenjie Zhao, Juan Wang, Yutian Lin, Wenwei Tu, Yurong Xiang, Ziyue Wu, Qiuji Yang, Shengwu Zhu, Sipin Li, Xiaoyang Notoginseng Triterpenes Inhibited Autophagy in Random Flaps via the Beclin-1/VPS34/LC3 Signaling Pathway to Improve Tissue Survival |
title | Notoginseng Triterpenes Inhibited Autophagy in Random Flaps via the Beclin-1/VPS34/LC3 Signaling Pathway to Improve Tissue Survival |
title_full | Notoginseng Triterpenes Inhibited Autophagy in Random Flaps via the Beclin-1/VPS34/LC3 Signaling Pathway to Improve Tissue Survival |
title_fullStr | Notoginseng Triterpenes Inhibited Autophagy in Random Flaps via the Beclin-1/VPS34/LC3 Signaling Pathway to Improve Tissue Survival |
title_full_unstemmed | Notoginseng Triterpenes Inhibited Autophagy in Random Flaps via the Beclin-1/VPS34/LC3 Signaling Pathway to Improve Tissue Survival |
title_short | Notoginseng Triterpenes Inhibited Autophagy in Random Flaps via the Beclin-1/VPS34/LC3 Signaling Pathway to Improve Tissue Survival |
title_sort | notoginseng triterpenes inhibited autophagy in random flaps via the beclin-1/vps34/lc3 signaling pathway to improve tissue survival |
topic | Bioengineering and Biotechnology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8640242/ https://www.ncbi.nlm.nih.gov/pubmed/34869285 http://dx.doi.org/10.3389/fbioe.2021.771066 |
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