Bafilomycin A1 Accelerates Chronic Refractory Wound Healing in db/db Mice.
Journal
BioMed research international
ISSN: 2314-6141
Titre abrégé: Biomed Res Int
Pays: United States
ID NLM: 101600173
Informations de publication
Date de publication:
2020
2020
Historique:
received:
26
03
2020
revised:
27
05
2020
accepted:
15
06
2020
entrez:
28
7
2020
pubmed:
28
7
2020
medline:
17
4
2021
Statut:
epublish
Résumé
Numerous studies have reported that autophagy plays an important role in chronic wound healing, and enhancement of autophagic activity impairs cutaneous wound healing. The autophagy inhibitor Bafilomycin A1 (Baf A1) inhibits autophagy by preventing the formation of autophagosomes. This study aimed at elucidating the effect of Bafilomycin A1 on chronic refractory wound healing in diabetic mice. A total of 40 diabetic (db/db) mice and 20 nondiabetic (db/m) mice were used in this study. Full-thickness skin defects were generated in the db/db mice models, which were then divided into the following two groups: the nontreated (db/db group) and Baf A1-treated groups (Baf A1 group). The same skin defects were generated in db/m mice (db/m group) to serve as a control. We demonstrated that Baf A1 treatment significantly accelerated wound healing in db/db mice and exerted good healing effects. Moreover, Baf A1 inhibited autophagy in the newly generated epidermis and had minor effects on metabolism in db/db mice. PCNA expression, as detected by immunohistochemistry, and collagen thickness, as detected by Masson's trichrome staining on the 14th day, were higher in the db/m and Baf A1 groups than in the db/db group. In addition, the expression of the proinflammatory cytokine TNF-
Identifiants
pubmed: 32714982
doi: 10.1155/2020/6265701
pmc: PMC7354638
doi:
Substances chimiques
Macrolides
0
Tumor Necrosis Factor-alpha
0
Interleukin-10
130068-27-8
bafilomycin A1
88899-55-2
Collagen
9007-34-5
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
6265701Informations de copyright
Copyright © 2020 Fan Wang et al.
Déclaration de conflit d'intérêts
The authors declare no conflicts of interest.
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