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

Figure 1

Neuroprotective effects of aescin treatment in vivo. (a) Primary neurons matured after 7 days from isolation. Neurons were subjected to 2 hours of OGD followed by 24 hours of reperfusion to simulate I/R injury in vitro. Neurons treated with aescin showed less axonotmesis compared with the OGD group. (b) LDH release was measured 24 hours after the experiments. All data after OGD and reperfusion were normalized to the values of the sham group (no OGD). After 2 hours of OGD and 24 hours of reperfusion, the LDH release ratio was significantly increased compared to the sham group. Aescin was administrated at various concentrations (5-100 μg/ml); treatments at concentrations of 25 μg/ml, 50 μg/ml, and 100 μg/ml aescin had protective effects in the form of reducing the LDH release induced by OGD and reperfusion compared with the no aescin treatment group (0 μg/ml). Neither 5 μg/ml nor 10 μg/ml aescin administration showed obviously protective effects, which means it worked in a dose-dependent manner. Furthermore, aescin at a concentration of 50 μg/ml resulted in a greater protective effect with less cytotoxicity after OGD and reperfusion. Values are . vs. sham (no OGD); ^# vs. no aescin treatment (0 μg/ml). per group.

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