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,...

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Veröffentlicht in:Jie fang jun yi xue za zhi 2018-01, Vol.43 (4), p.310
Hauptverfasser: Jian-xiong, LI, Ming-ming, LI, Yu-jie, BU, LI, Bin, ZOU, Hua, Ting-hua, ZHANG
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container_issue 4
container_start_page 310
container_title Jie fang jun yi xue za zhi
container_volume 43
creator Jian-xiong, LI
Ming-ming, LI
Yu-jie, BU
LI, Bin
ZOU, Hua
Ting-hua, ZHANG
description 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
doi_str_mv 10.11855/j.issn.0577-7402.2018.04.08
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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. 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Proteins
title Effects of 17-AAG on neurons apoptosis induced by oxygen-glucose deprivation and recovery
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