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Some scholars have suggested that the clinical application of exosomes derived from human umbilical cord mesenchymal stem cells (hucMSCs-exo) might represent a novel strategy to improve diabetic wound healing. However, the mechanisms underlying the effects of hucMSCs-exo on wound healing remain poorly understood. This study aimed to identify the mechanism of hucMSCs-exo in treating diabetic wounds. HucMSCs-exo were isolated from human umbilical cord mesenchymal stem cells (hucMSCs) and subcutaneously injected into full-thickness wounds in diabetic rats. Wound healing closure rates and histological analysis were performed. The levels of tumor necrosis factor-α (TNF-α), macrophage mannose receptor (MMR/CD206), platelet endothelial cell adhesion molecule-1 (PECAM-1/CD31), and vascular endothelial growth factor (VEGF) were detected by immunohistochemistry. The degree of collagen deposition was examined using Masson’s trichrome staining. Gross evaluation of wound healing was carried out from day 0 to 14 post-surgery, and the wound site was harvested for histology on days 3, 7, and 14 post-wounding. HucMSCs-exo transplantation increased diabetic wound healing. In vitro, hucMSCs-exo promoted the proliferation of human umbilical vein endothelial cells (HUVECs) and NIH-3T3 cells. In vivo, hucMSCs-exo reduced wound area and inflammatory infiltration and increased collagen fibers. In addition, wound tissues in the hucMSCs-exo group had higher CD206, CD31, and VEGF expressions and lower TNF-α levels than those in the control group on day 14. Our results demonstrated that hucMSCs-exo facilitated diabetic wound repair by inducing anti-inflammatory macrophages and promoting angiogenesis and collagen deposition.

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Emerging evidence has indicated that mesenchymal stem cells (MSCs) are involved in the modulation of inflammation. Human placenta-derived (HPL)-MSCs exist in sufficient quantities and play a role in immune regulation. However, the exact roles of HPL-MSCs in inflammation and the specific underlying mechanisms are not well defined. In the present study, HPL-MSCs were obtained from human fetal placentas, and further purified using a commercial kit. Using ELISA, reverse transcription-quantitative PCR, western blot, NO detection and other assays, the present study revealed that HPL-MSCs may improve lipopolysaccharide-induced macrophage inflammation by regulating macrophage polarization. Further mechanistic studies demonstrated that HPL-MSCs attenuated the NF-κB signaling pathway by regulating the expression of toll-like receptor 4 and the phosphorylation of IκBα and p65, which resulted in a reduction in the levels of inflammation. The present study indicated that HPL-MSCs may act as a novel target for the treatment of inflammation-related diseases.