Abstract

Diabetic wounds exhibit retarded and partial healing processes. Therefore, patients are exposed to an elevated risk of infection. It has been verified that Angelica dahurica (Hoffm.) Benth. and Hook. f. ex Franch. and Sav (A. dahurica) is conducive for wound healing. However, the pharmacological mechanisms of A. dahurica are yet to be established. The present study uses network pharmacology and in vivo experimental validation to investigate the underlying process that makes A. dahurica conducive for faster wound healing in diabetes patients. 54 potential targets in A. dahurica that act on wound healing were identified through network pharmacology assays, such as signal transducer and activator of transcription 3 (STAT3), JUN, interleukin-1β (IL-1β), tumor necrosis factor (TNF), and prostaglandin G/H synthase 2 (PTGS2). Furthermore, in vivo validation showed that A. dahurica accelerated wound healing through anti-inflammatory effects. More specifically, it regulates the polarization of M1 and M2 subtypes of macrophages. A. dahurica exerted a curative effect on diabetic wound healing by regulating the inflammation. Hence, pharmacologic network analysis combined with in vivo validation elucidated the probable effects and underlying mechanisms of A. dahurica’s therapeutic effect on diabetic wound healing.

Highlights

  • A wound heals in a natural reparative process

  • Once the compounds were collected from the TCMSP database, they were converted into the UniProt database and the redundant items were deleted

  • This study indicated a novel mechanism of the A. dahurica that accelerates diabetic wound healing through a network pharmacology and experimental validation

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Summary

Introduction

A wound heals in a natural reparative process. It is the process through which the body responds to tissue injuries. Failing to advance these four stages in an orderly manner results in impaired wound healing, representing one of the primary causes of fatalities associated with diabetes. It affects nearly 25% of diabetes patients (Armstrong et al, 2017). Such wounds often become points of entry for bacterial

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