ACSL4 contributes to sevoflurane-induced ferroptotic neuronal death in SH-SY5Y cells via the 5' AMP-activated protein kinase/mammalian target of rapamycin pathway.

ABSTRACT:

Background

Acyl-CoA synthetase long chain family member 4 (ACSL4) has been reported to serve as a major player in the progress of ferroptosis in various diseases. Nevertheless, the functional role and mechanism of ACSL4 in sevoflurane (sev)-induced neuronal death has never been elucidated.

Methods

Cell viability was assessed using Cell Counting Kit-8 (CCK-8). Iron levels, reactive oxygen species (ROS) production, and malondialdehyde (MDA), 4-hydroxynonenal (4-HNE), and glutathione (GSH) content were determined to assess ferroptosis level. Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and western blot were undertaken for the measurement of gene expression.

Results

Sev hindered the viability of SH-SY5Y cells and suppression

SUBMITTER: Cheng L 

PROVIDER: S-EPMC8506733 | biostudies-literature | 2021 Sep

REPOSITORIES: biostudies-literature