Effects of 17-AAG on neurons apoptosis induced by oxygen-glucose deprivation and recovery

Objective To explore the role and mechanism of 17-allylamino-17-demethoxygeldanamycin (17-AAG) in neurons apoptosis induced by oxygen-glucose deprivation and recovery (OGD/R). Methods Primary rat neurons were cultivated in vitro, and OGD/R model was reproduced. Neurons were exposed to OGD for 0.5h, 1h and 2h, and then reperfusion for 24h, the effect of OGD/R on neurons apoptosis was detected by TUNEL assay. On OGD/R, neurons were treated with different concentrations of 17-AAG (0.5, 1.0 and 2.0μmol/L), and the effect of 17-AAG on OGD/R treated neurons apoptosis was detected by TUNEL assay. Western blotting was performed to detect the expression of heat shock protein 70 (HSP70). HSP70 interference lentivirus was then constructed. The effect of HSP70 interference on the neurons apoptosis treated with OGD/R and 17-AAG was detected by TUNEL assay. Results OGD/R significantly induced neurons apoptosis, and the rate of neurons apoptosis increased with the increase of OGD time. 17-AAG obviously inhibited the neurons