研究动态
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通过局部应用大卡尔瓦提亚提取物重塑共生伤口微生物群,有助于更快的糖尿病伤口愈合。

Reshaped commensal wound microbiome via topical application of Calvatia gigantea extract contributes to faster diabetic wound healing.

发表日期:2024
作者: Xiaotong Ding, Chenxi Yang, Yue Li, Tangtang He, Yan Xu, Xuxi Cheng, Jinyun Song, Nannan Xue, Wen Min, Weimeng Feng, Hongyu Zhao, Jie Dong, Pei Liu, Yiwei Wang, Jun Chen
来源: CYTOKINE & GROWTH FACTOR REVIEWS

摘要:

Calvatia gigantea (CG) 被广泛用作伤口治疗的中药。在本研究中,我们旨在确定CG提取物(CGE)对糖尿病伤口愈合和共生伤口微生物群的影响。使用瘦素受体缺陷的db/db小鼠建立伤口模型,以未治疗的小鼠为对照组,CGE -将小鼠作为治疗组。分析伤口愈合率、炎症和组织学。此外,通过 16S 核糖体 RNA (rRNA) 基因测序评估伤口微生物组。CGE 显着加速糖尿病溃疡伤口的愈合,促进上皮细胞再形成,并下调炎症细胞因子、白介素-1β 和肿瘤坏死因子-α 的转录水平。此外,CGE 治疗对伤口微生物组产生积极影响,促进 CGE 治疗组微生物群落的多样性和埃希氏菌-志贺氏菌的富集。总体而言,CGE 通过调节伤口微生物组和促进炎症期间巨噬细胞极化来增强糖尿病伤口愈合。这些发现表明,使用药用植物调节共生伤口微生物组作为糖尿病伤口的潜在治疗策略。© 作者 2024。由牛津大学出版社出版。
Calvatia gigantea (CG) is widely used as a traditional Chinese medicine for wound treatment. In this study, we aimed to determine the effects of CG extract (CGE) on diabetic wound healing and the commensal wound microbiome.A wound model was established using leptin receptor-deficient db/db mice, with untreated mice as the control group and CGE-treated mice as the treatment group. The wound healing rate, inflammation and histology were analyzed. Additionally, wound microbiome was evaluated via 16S ribosomal RNA (rRNA) gene sequencing.CGE significantly accelerated the healing of diabetic ulcer wounds, facilitated re-epithelialization, and downregulated the transcription levels of the inflammatory cytokines, interleukin-1β and tumor necrosis factor-α. Furthermore, CGE treatment positively affected the wound microbiome, promoting diversity of the microbial community and enrichment of Escherichia-Shigella bacteria in the CGE-treated group.Overall, CGE enhanced diabetic wound healing by modulating the wound microbiome and facilitating macrophage polarization during inflammation. These findings suggest modulation of the commensal wound microbiome using medicinal plants as a potential therapeutic strategy for diabetic wounds.© The Author(s) 2024. Published by Oxford University Press.