Formononetin alleviates thermal injury-induced skin fibroblast apoptosis and promotes cell proliferation and migration.

The aim of this study was to explore the effect and mechanism of formononetin (FMNT) in thermal-injured fibroblast proliferation, apoptosis, and oxidative stress. After thermal injury, human skin fibroblast (HSF) cells showed inhibited proliferation, migration, extracellular matrix (ECM) synthesis; and increased apoptosis, reactive oxygen species (ROS) production, and inflammation. Specifically, after thermal injury, cell viability, migration distance, and protein levels of collagen I, collagen III, α-SMA, MMP1, and MMP3 were reduced; cell apoptosis rate and TUNEL-positive cell numbers were increased; the levels of Bax and cleaved caspase-3 were elevated, while Bcl-2 level was reduced.

miR-506-3p regulates TGF- 1 and affects dermal fibroblast proliferation, migration and collagen formation after thermal injury.

Dermal fibroblasts are a promising candidate for cellular-based therapies for thermal wound healing because of their capacity of producing extracellular matrix (ECM), promoting wound contraction and the synthesis of type I collagen, and secreting growth factors. miRNAs (MicroRNAs) might mediate the role of TGF-β1(Transforming Growth Factor-beta 1), one of the major profibrotic cytokines, in improving thermal injury repair. In the present study, we observed the abnormal downregulation of TGF-β1 following thermal injury in the burnt dermis (in vivo) and heat-stimulated human dermal fibroblasts (in vitro).