FGF21 promotes wound healing of rat brain microvascular endothelial cells through facilitating TNF-α-mediated VEGFA and ERK1/2 signaling pathway

Background Wound healing is an essential physiological process in recovery after microsurgery. Objectives To further understand the functions of fibroblast growth factor 21 (FGF21), roles this were examined and its correlations with inflammation, vascular endothelial A (VEGFA) ERK1/2 signaling pathway activation analyzed. Material methods Rat brain microvascular cells (RBMECs) treated interleukin (IL)-1β used for experiments. Cell Counting Kit-8 (CCK-8) was to detect cell viability RBMECs treatment IL-1β (1 ng/mL) FGF21 or VEGFA overexpression, while changes apoptosis measured through flow cytometry. Migration checked scratch test. RNA expression assessed using reverse-transcription quantitative polymerase chain reaction (RT-qPCR), which also examine Bcl-2, Bax caspase-3. After tumor necrosis alpha (TNF-α) β1 (TGF-β1) proteins level observed enzyme-linked immunosorbent assay (ELISA), applied check overexpression VEGFA. PD98059 (50 μM), inhibitor, regulating apoptosis. Results The significantly decreased TGF-β1, but promoted TNF-α expression. downregulated by enhanced TGF-β1 protein levels, attenuated TNF-α. Upregulated restrained upregulation not only suppressed FGF21, Moreover, suppression increased upregulation. However, obstructed Conclusions upregulating TNF-α-mediated signaling.