Neuroprotective effects of 1-O-hexyl-2,3,5-trimethylhydroquinone on ischaemia/reperfusion-induced neuronal injury by activating the Nrf2/HO-1 pathway.
Animals
Antioxidants
/ metabolism
Apoptosis
/ drug effects
Heme Oxygenase-1
/ metabolism
Hydroquinones
/ pharmacology
Male
Mice, Inbred C57BL
NF-E2-Related Factor 2
/ metabolism
Neurons
/ drug effects
Neuroprotective Agents
/ pharmacology
Oxidative Stress
/ drug effects
PC12 Cells
Rats
Reperfusion Injury
/ drug therapy
Signal Transduction
1-O-Hexyl-2,3,5-trimethylhydroquinone
HO-1
Nrf2
PC12 cells
cerebral ischaemic/reperfusion
Journal
Journal of cellular and molecular medicine
ISSN: 1582-4934
Titre abrégé: J Cell Mol Med
Pays: England
ID NLM: 101083777
Informations de publication
Date de publication:
09 2020
09 2020
Historique:
received:
18
09
2019
revised:
29
04
2020
accepted:
29
06
2020
pubmed:
18
7
2020
medline:
8
5
2021
entrez:
18
7
2020
Statut:
ppublish
Résumé
1-O-Hexyl-2,3,5-trimethylhydroquinone (HTHQ), a lipophilic phenolic agent, has an antioxidant activity and reactive oxygen species (ROS) scavenging property. However, the role of HTHQ on cerebral ischaemic/reperfusion (I/R) injury and the underlying mechanisms remain poorly understood. In the present study, we demonstrated that HTHQ treatment ameliorated cerebral I/R injury in vivo, as demonstrated by the decreased infarct volume ration, neurological deficits, oxidative stress and neuronal apoptosis. HTHQ treatment increased the levels of nuclear factor erythroid 2-related factor 2 (Nrf2) and its downstream antioxidant protein, haeme oxygenase-1 (HO-1). In addition, HTHQ treatment decreases oxidative stress and neuronal apoptosis of PC12 cells following hypoxia and reperfusion (H/R) in vitro. Moreover, we provided evidence that PC12 cells were more vulnerable to H/R-induced oxidative stress after si-Nrf2 transfection, and the HTHQ-mediated protection was lost in PC12 cells transfected with siNrf2. In conclusion, these results suggested that HTHQ possesses neuroprotective effects against oxidative stress and apoptosis after cerebral I/R injury via activation of the Nrf2/HO-1 pathway.
Identifiants
pubmed: 32677362
doi: 10.1111/jcmm.15659
pmc: PMC7521305
doi:
Substances chimiques
Antioxidants
0
Hydroquinones
0
NF-E2-Related Factor 2
0
Neuroprotective Agents
0
1-O-hexyl-2,3,5-trimethylhydroquinone
70BK60I8RP
Heme Oxygenase-1
EC 1.14.14.18
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
10468-10477Informations de copyright
© 2020 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.
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