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

Wu Xiong, Xue Bai, Xi Zhang, Huajuan Lei, Hui Xiao, Luyao Zhang, Yuting Xiao, Qianpei Yang, Xiaoling Zou
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Abstract

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 αSMA- 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.
黄芪甲苷诱导的内皮祖细胞衍生外泌体通过PI3K/AKT/mTOR通路加速大鼠I型糖尿病伤口愈合
目的:探讨内皮祖细胞(EPC)衍生外泌体(EPCexos)和黄芪甲苷(ASIV)刺激的EPCexos (ASIV-EPCexos)对I型糖尿病创面愈合的影响,并确定其作用的基本分子机制。方法:将EPCs暴露于不同浓度的asv中,产生asv - epceos。建立链脲佐菌素刺激的糖尿病大鼠慢性创面愈合模型。这些大鼠分别用EPCexos、ASIV-EPCexos、雷帕霉素和wortmannin治疗。采用直接摄影观察、苏木精、伊红染色、马松三色染色评价创面愈合情况。结果:asv处理增加了EPCs的能力(如增殖),以及外泌体的分泌。EPCexo呈“杯托”状结构。用asiv - epceos治疗可增加创面愈合率、胶原沉积面积、溴脱氧尿苷吸收、VEGF表达、CD31和αSMA阳性细胞数量,同时降低表皮厚度和CD45表达。PI3K/AKT/mTOR通路表达升高,炎性因子表达降低。然而,雷帕霉素和沃特曼宁逆转了这些变化。结论:asiv - epceos可能通过PI3K/AKT/mTOR通路加速I型糖尿病伤口愈合。本研究可能为1型糖尿病创面的临床治疗提供新的选择。
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