Fig. 1.

(A) BG acts on neutrophils, increasing free radicals and promoting wound activation. BG can be phagocytic by macrophages, promote adhesion and extension of macrophages, and up-regulate TNF-α. BG acts on macrophages to regulate their cytokine secretion, and when macrophages are activated as M1 macrophages, TNF-α, IL-6, and IL-10 are down-regulated. BG can regulate the phenotype of macrophages, inhibit the inflammatory response, reduce the activity expression of M1 macrophages, reduce inflammation, activate the transformation of macrophages to M2, express more anti-inflammatory factors, promote angiogenesis, up-regulate GPX4 expression, clear excess ROS, and improve mitochondrial function. (B) BG induces the expression of TGF-β and PDGF in fibroblasts, and the high expression of bFGF, VEGF, and Col I can promote endothelial cell proliferation and accelerate the process of angiogenesis, which regulates the activity of light and heat and nitric oxide release, promoting the proliferation of fibroblasts; BG also down-regulates collagen synthesis and fibroblast differentiation into myofibroblasts via the TGF-β1–Smad2 signaling pathway. BG can promote endothelial cell gap junction, promote CX43 expression, and accelerate the process of neovascularization. ADSCs self-renew and differentiate into keratinocytes, DFs, and cells in the basal layer, and they show strong migration and recruitment ability to the injured site. BG can enhance the adhesion of ADSC stem cells. BG pretreatment enhanced the therapeutic ability of mesenchymal stem cell-derived extracellular vesicle (MSC-EV) and significantly up-regulated functional substances such as miR-199b-3p and miR-125a-5p.