Endothelial Progenitor-Cell-Derived Exosomes Induced by Astragaloside IV Accelerate Type I Diabetic-wound Healing via the PI3K/AKT/mTOR Pathway in Rats

被引:9
作者
Xiong, Wu [1 ]
Bai, Xue [2 ]
Zhang, Xi [3 ,4 ]
Lei, Huajuan [5 ]
Xiao, Hui [2 ]
Zhang, Luyao [6 ]
Xiao, Yuting [6 ]
Yang, Qianpei [6 ]
Zou, Xiaoling [2 ]
机构
[1] Hunan Univ Chinese Med, Affiliated Hosp 1, Dept Burns & Plast Surg, Changsha 410007, Hunan, Peoples R China
[2] Hunan Univ Chinese Med, Affiliated Hosp 1, Dept Endocrinol, Changsha 410007, Hunan, Peoples R China
[3] Hunan Prov Brain Hosp, Dept Sci Res, Changsha 410007, Hunan, Peoples R China
[4] Hunan Univ Chinese Med, Clin Med Sch, Changsha 410007, Hunan, Peoples R China
[5] Hunan Univ Chinese Med, Affiliated Hosp 1, Dept Anesthesiol, Changsha 410007, Hunan, Peoples R China
[6] Hunan Univ Chinese Med, Coll Integrated Tradit Chinese & Western Med, Changsha 410208, Hunan, Peoples R China
来源
FRONTIERS IN BIOSCIENCE-LANDMARK | 2023年 / 28卷 / 11期
基金
湖南省自然科学基金; 中国国家自然科学基金;
关键词
astragaloside IV; PI3K/AKT/mTOR; endothelial progenitor cells; exosome; angiogenesis; OXIDATIVE STRESS; FOOT ULCER; ANGIOGENESIS; INFLAMMATION; MELLITUS;
D O I
10.31083/j.fbl2811282
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Objective: We explore the effects of endothelial progenitor cell (EPC)-derived exosomes (EPCexos) and of astragaloside IV (ASIV)stimulated EPCexos (ASIV-EPCexos) on type I diabetic-wound healing, and determine the basic molecular mechanisms of action. Methods: EPCs were exposed to different concentrations of ASIV to generate ASIV-EPCexos. A chronic-wound healing model involving streptozotocin-stimulated diabetic rats was established. These rats were treated with EPCexos, ASIV-EPCexos, rapamycin, and wortmannin. Wound healing was evaluated by direct photographic observation, hematoxylin and eosin staining, and Masson's trichrome staining. Results: ASIV treatment increased the abilities of EPCs (e.g., proliferation), as well as exosome secretion. EPCexo showed a "cup holder" like structure. Treatment with ASIV-EPCexos increased the wound-healing rate, collagen-deposition area, bromodeoxyuridine uptake, VEGF expression, and the number of CD31- and alpha SMA- positive cells, whereas decreased epidermal thickness and CD45 expression. The expression of the PI3K/AKT/mTOR pathway increased, whereas the expression of inflammatory factor decreased. However, rapamycin and wortmannin reversed these changes. Conclusions: ASIV-EPCexos may accelerate type I diabetic-wound healing via the PI3K/AKT/mTOR pathway. This study may lay the foundation for new clinical treatment options for patients with type I diabetic wounds.
引用
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页数:14
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