Astragalus Polysaccharides Promote Skin Wound Healing by Regulating the miR-92a/FGF2 Axis
Description
This study investigates APS regulation of fibroblast behavior via the miR-92a/FGF2 axis using FISH, WB, qPCR, functional assays, and RNA-seq. APS significantly enhanced HFF-1 proliferation/migration (p<0.01), upregulated FGF2, and suppressed miR-92a. Mechanistically, miR-92a directly targeted FGF2 3'UTR (luciferase/FISH), inhibiting fibroblast activation. miR-92a overexpression blunted APS effects, while its inhibition rescued them. In rat wounds, APS accelerated closure by 40% (p<0.001) and elevated FGF2, whereas miR-92a mimics impaired healing. RNA-seq identified 23 miR-92a/FGF2-regulated ECM reorganization targets. Collectively, APS promotes repair by suppressing miR-92a to activate FGF2—establishing miR-92a as a therapeutic checkpoint for enhancing APS-driven regeneration.