Aescin Protects Neuron from Ischemia-Reperfusion Injury via Regulating the PRAS40/mTOR Signaling Pathway

Figure 2

Aescin treatments upregulated the phosphorylation of PRAS40, mTOR, S6K, and 4E-BP1 in neurons after OGD and reperfusion. (a) Representative protein bands of critical molecules in the PRAS40/mTOR pathways were measured by western blot. The results showed the protein bands of phosphorylated and nonphosphorylated PRAS40, mTOR, S6K, and 4E-BP1 after 2 hours of OGD followed by 24 hours of reperfusion with 50 μg/ml aescin treatment or without aescin treatment in primary cultured neurons. Protein bands of the sham group (no OGD) were also displayed. β-Actin was used as a control to ensure equal protein loading. (b) The bar graphs represented the relative quantified protein levels of the phosphorylated and nonphosphorylated PRAS40, mTOR, S6K, and 4E-BP1, respectively. All results are given as . vs. sham (no OGD); ^# vs. aescin treatment (50 μg/ml). per group. Sham group: no OGD samples; Con group: OGD/R samples without treatment; NS group: OGD/R samples treated with normal saline; aescin group: OGD/R samples treated with aescin.

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