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. 2019 Aug 30;36(18):2676–2687. doi: 10.1089/neu.2018.6294

FIG. 3.

FIG. 3.

Bisperoxovanadium (bpV) activated prosurvival kinase/mammalian target of rapamycin (Akt/mTOR) in injured spinal neurons in vitro. (A) Scratch injury induced a decrease in Akt phosphorylation that was significantly reversed by bpV treatment. Application of a PI3K inhibitor LY294002 diminished Akt phosphorylation in the presence of bpV. (B) Ribosomal protein S6 phosphorylation, a marker of mTOR activity, significantly increased after scratch injury as observed in vivo. Treatment with bpV significantly increased p-S6 expression over scratch-induced injury alone. Treatment with an mTOR inhibitor, rapamycin, reduced S6 phosphorylation post-scratch injury and bpV treatment. Data were expressed as mean ± standard error of the mean; n = 3–4 experiments; All data analyzed via one-way analysis of variance; *p < 0.05; **p < 0.01; ***p < 0.001.