Neuroprotective effect of deferoxamine on erastininduced ferroptosis in primary cortical neurons.

Abstract:

:The iron chelator deferoxamine has been shown to inhibit ferroptosis in spinal cord injury. However, it is unclear whether deferoxamine directly protects neurons from ferroptotic cell death. By comparing the survival rate and morphology of primary neurons and SH-SY5Y cells exposed to erastin, it was found that these cell types respond differentially to the duration and concentration of erastin treatment. Therefore, we studied the mechanisms of ferroptosis using primary cortical neurons from E16 mouse embryos. After treatment with 50 μM erastin for 48 hours, reactive oxygen species levels increased, and the expression of the cystine/glutamate antiporter system light chain and glutathione peroxidase 4 decreased. Pretreatment with deferoxamine for 12 hours inhibited these changes, reduced cell death, and ameliorated cellular morphology. Pretreatment with the apoptosis inhibitor Z-DEVD-FMK or the necroptosis inhibitor necrostain-1 for 12 hours did not protect against erastin-induced ferroptosis. Only deferoxamine protected the primary cortical neurons from ferroptosis induced by erastin, confirming the specificity of the in vitro ferroptosis model. This study was approved by the Animal Ethics Committee at the Institute of Radiation Medicine of the Chinese Academy of Medical Sciences, China (approval No. DWLL-20180913) on September 13, 2018.

journal_name

Neural Regen Res

authors

Zhang Y,Fan BY,Pang YL,Shen WY,Wang X,Zhao CX,Li WX,Liu C,Kong XH,Ning GZ,Feng SQ,Yao X

doi

10.4103/1673-5374.274344

subject

Has Abstract

pub_date

2020-08-01 00:00:00

pages

1539-1545

issue

8

eissn

1673-5374

issn

1876-7958

pii

NeuralRegenRes_2020_15_8_1539_274344

journal_volume

15

pub_type

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