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

Figure 4

The effects of PRAS40 knockdown after OGD and reperfusion in vivo. (a) Primary cultured neurons were transfected with lentivirus containing PRAS40 shRNA 4 days before experiments; the control group was transfected with vectors expressing GFP. Then, they were subjected to the same OGD and reperfusion procedures. The LDH release represented neuronal death was measured by the same method. (b) PRAS40 knockdown (PRAS40 KD) did inhibit the expression of pmTOR, pS6K, and p4E-BP1 obviously. Representative western blot results showed the protein bands in the PRAS40/mTOR pathways, including phosphorylated and nonphosphorylated protein levels. (c) The bar graphs showed the relatively quantified protein levels of pPRAS40, PRAS40, pmTOR, mTOR, pS6K, S6K, p4E-BP1, and 4E-BP1, respectively. All results are given as . vs. sham (no OGD); ^# vs. PRAS40 KD; vs. PRAS40 KD. per group. Sham group: no OGD samples; Con group: OGD/R samples without treatment; vector group: OGD/R samples treated with empty vector; PRAS40 KD group: OGD/R samples treated with PRAS40 shRNA.

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