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-α in the db/m and Baf A1 groups increased significantly on day 6, and the expression of the anti-inflammatory cytokine IL-10 also increased significantly on day 9. However, there were no significant changes in the expression levels of TNF-α and IL-10 in the db/db group. Therefore, Baf A1 may accelerate diabetic chronic refractory wound healing by promoting cell proliferation, collagen production, and regulating the inflammatory balance.

中文翻译：

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Bafilomycin A1促进db / db小鼠的慢性难治性伤口愈合。

许多研究报道自噬在慢性伤口愈合中起重要作用，自噬活性的增强会损害皮肤伤口的愈合。自噬抑制剂Bafilomycin A1（Baf A1）通过阻止自噬小体的形成来抑制自噬。这项研究旨在阐明Bafilomycin A1对糖尿病小鼠慢性难治性伤口愈合的作用。本研究共使用40只糖尿病（db / db）小鼠和20只非糖尿病（db / m）小鼠。在db / db小鼠模型中产生了全层皮肤缺陷，然后将其分为以下两组：未治疗组（db / db组）和Baf A1治疗组（Baf A1组）。在db / m小鼠（db / m组）中产生了相同的皮肤缺损，以作为对照。我们证明，Baf A1治疗可显着加速db / db小鼠的伤口愈合并发挥良好的愈合作用。此外，Baf A1抑制了新生表皮中的自噬，并且对db / db小鼠的新陈代谢影响很小。通过db / m和Baf A1组，通过免疫组织化学检测到的PCNA表达和在第14天通过Masson三色染色检测到的胶原蛋白厚度均高于db / db组。另外，促炎细胞因子TNF-α的表达 在db / m和Baf A1组中高于在db / db组中。另外，促炎细胞因子TNF-α的表达 在db / m和Baf A1组中高于在db / db组中。另外，促炎细胞因子TNF-α的表达db / m组和Baf A1组中的α在第6天显着增加，而抗炎细胞因子IL-10的表达在第9天也显着增加。但是，TNF- α的表达水平没有明显变化。和db / db组中的IL-10。因此，Baf A1可通过促进细胞增殖，胶原蛋白生成和调节炎症平衡来加速糖尿病慢性难治性伤口愈合。