Quercetin inhibits the migration and proliferation of astrocytes in wound healing

A previous study showed that quercetin inhibits astrogliosis in a scratch-wound model, but did not identify the underlying mechanisms. Here, we show that quercetin exerts no effect on apoptosis or the viability of astrocytes, but significantly inhibits their proliferation, arresting them in the G1phase and decreasing the percentage of cells in the S and G2phase. In addition, we found that quercetin significantly decreased the phosphorylation of ERK12 and FAK, a downstream ERK signaling protein. Inhibition of this pathway with U0126, an inhibitor of MAP kinase, retarded wound closure, whereas sustained p-ERK12 activation, induced by vanadate, restored astrocyte migration. Our findings thus indicate that quercetin inhibits healing in the scratch-wound model of primary astrocytes in two ways: blockade of the G1to S phase cell cycle transition and inhibition of the ERKFAK signaling pathway, which may contribute toward decreasing astroglial scar formation in vivo.