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4-羟基苯甲醛通过激活角质细胞中的粘着斑信号加速急性伤口愈合。

4-Hydroxybenzaldehyde accelerates acute wound healing through activation of focal adhesion signalling in keratinocytes.

机构信息

Brain Korea 21 PLUS Project for Medical Science, Yonsei University, Seoul, Korea.

Endocrinology, Institute of Endocrine Research, College of Medicine, Yonsei University, Seoul, Korea.

出版信息

Sci Rep. 2017 Oct 27;7(1):14192. doi: 10.1038/s41598-017-14368-y.

DOI:10.1038/s41598-017-14368-y
PMID:29079748
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5660242/
Abstract

4-Hydroxybenzaldehyde (4-HBA) is a naturally occurring benzaldehyde and the major active constituent of Gastrodia elata. While recent studies have demonstrated metabolic effects of 4-HBA, little is known about the physiological role of 4-HBA in acute wound healing. Here, we investigated the effects and mechanisms of 4-HBA on acute wound healing. Using an in vitro approach, we found that 4-HBA significantly promoted keratinocyte cell migration and invasion by increasing focal adhesion kinase and Src activity. In addition, 4-HBA treatment also promoted wound healing and re-epithelialization in an in vivo excision wound animal model. Combination treatment with 4-HBA and platelet-derived growth factor subunit B homodimer showed synergistic effects in promoting wound healing. Taken together, our results demonstrated that treatment with 4-HBA promoted keratinocyte migration and wound healing in mouse skin through the Src/mitogen-activated protein kinase pathway. Therefore, 4-HBA could be a candidate therapeutic agent with the potential to promote acute wound healing.

摘要

4-羟基苯甲醛(4-HBA)是一种天然存在的苯甲醛,也是天麻的主要活性成分。虽然最近的研究表明 4-HBA 具有代谢作用,但对于其在急性伤口愈合中的生理作用知之甚少。在这里,我们研究了 4-HBA 对急性伤口愈合的影响及其机制。通过体外方法,我们发现 4-HBA 通过增加粘着斑激酶和Src 活性,显著促进角质形成细胞的迁移和侵袭。此外,4-HBA 处理还促进了体内切除伤口动物模型中的伤口愈合和再上皮化。4-HBA 与血小板衍生生长因子亚基 B 同二聚体联合治疗显示出协同促进伤口愈合的作用。总之,我们的结果表明,4-HBA 通过Src/丝裂原活化蛋白激酶途径促进角质形成细胞迁移和小鼠皮肤伤口愈合。因此,4-HBA 可能是一种有潜力促进急性伤口愈合的候选治疗药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8167/5660242/a83194ccaed5/41598_2017_14368_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8167/5660242/834b050a2c24/41598_2017_14368_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8167/5660242/43a91c19f99f/41598_2017_14368_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8167/5660242/0921779ccdde/41598_2017_14368_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8167/5660242/a9b1454be058/41598_2017_14368_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8167/5660242/a83194ccaed5/41598_2017_14368_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8167/5660242/834b050a2c24/41598_2017_14368_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8167/5660242/43a91c19f99f/41598_2017_14368_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8167/5660242/0921779ccdde/41598_2017_14368_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8167/5660242/a9b1454be058/41598_2017_14368_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8167/5660242/a83194ccaed5/41598_2017_14368_Fig5_HTML.jpg

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