4.7 Article

Identification of active compounds and molecular mechanisms of Dalbergia tsoi Merr.et Chun to accelerate wound healing

期刊

BIOMEDICINE & PHARMACOTHERAPY
卷 150, 期 -, 页码 -

出版社

ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
DOI: 10.1016/j.biopha.2022.112990

关键词

Dalbergia tsoi Merr.et Chun; Wound healing; UPLC-Q-Orbitrap HRMS; PI3K/Akt signaling pathway; Network pharmacology; Molecular docking

资金

  1. National Natural Science Foundation of China [82141211, 82174043]
  2. Guangdong Basic and Applied Basic Research Foundation [2021A1515011697]
  3. High tech Industrialization Entrepreneurship Team Project of Foshan High-tech Zone [2120197000214]
  4. Innovation and Entrepreneurship Team Project Introduced by Shunde District, Foshan City [2130218004133]
  5. Characteristic innovation research project of college teachers

向作者/读者索取更多资源

This study explored the effects, active compounds, and molecular mechanisms of Dalbergia tsoi Merr.et Chun (JZX) in wound healing. The results showed that JZX accelerated wound healing, improved tissue quality, and inhibited inflammation and oxidative stress. The active compounds butin, eriodyctiol, and formononetin were identified as the key compounds in facilitating wound treatment. JZX accelerated wound healing by regulating the PI3K/Akt signaling pathway and inducing the expression of growth factors.
As a traditional Chinese medicine, Dalbergia tsoi Merr.et Chun (JZX) has been used for the treatment of wounds since ancient times. However, the active compounds and molecular mechanisms of JZX in the acceleration of wound healing are still unknown. Herein, we explored the main active compounds and key molecular mechanisms by which JZX accelerates wound healing. The ethanol extract of JZX was subjected to UPLC-Q-Orbitrap HRMS analysis to identify the main compounds. The pharmacological effect of JZX on wound healing was evaluated using a mouse excision wound model. Network pharmacology was utilized to predict the effective compounds and related signal transduction pathways of JZX that were involved in accelerating wound healing. The predicted key signaling pathways were then validated by immunohistochemical analysis. Interactions between the active compounds and therapeutic targets were confirmed by molecular docking analysis. JZX accelerated wound healing, improved tissue quality, and inhibited inflammation and oxidative stress. Moreover, our results suggested that the active components of JZX, such as butin, eriodyctiol, and formononetin, are the key compounds that facilitate wound treatment. Our studies also indicated that JZX accelerated wound healing by regulating the PI3K/Akt signaling pathway and inducing the expression of TGF-beta 1, FGF2, VEGFA, ECM1, and alpha-SMA at different stages of skin wound healing. The JZX extract accelerates wound healing by reducing inflammation and inhibiting oxidative stress, regulating the PI3K/Akt signaling pathway, and promoting the expression of growth factors, suggesting that JZX has potential clinical applicability in wound treatment.

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