Melatonin improves hypoxic-ischemic brain damage through the Akt/Nrf2/Gpx4 signaling pathway.

Abstract:

:Melatonin (Mel) has neuroprotective effects; however, its roles in hypoxic-ischemic brain damage (HIBD) and the underlying mechanisms remain unknown. We aimed to explore its roles and mechanisms in a HIBD rat model. We found that exogenous Mel treatment ameliorated HIBD-induced pathological changes, inhibited neuronal ferroptosis, and promoted hippocampal neuronal survival. Moreover, Mel improved the learning and memory abilities of the HIBD rats. Further, we found that glutathione peroxidase 4 (Gpx4) inhibition with RSL3, Akt inhibition with LY29400, and nuclear factor erythroid-2-related factor 2 (Nrf2) inhibition with ML385 abolished the Mel protective effects in HIBD. Our findings indicate that exogenous Mel treatment has a protective effect on HIBD via the Akt/Nrf2/Gpx4 pathway.

journal_name

Brain Res Bull

journal_title

Brain research bulletin

authors

Gou Z,Su X,Hu X,Zhou Y,Huang L,Fan Y,Li J,Lu L

doi

10.1016/j.brainresbull.2020.07.011

subject

Has Abstract

pub_date

2020-10-01 00:00:00

pages

40-48

eissn

0361-9230

issn

1873-2747

pii

S0361-9230(20)30558-X

journal_volume

163

pub_type

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