Neuroprotective role of Nrf2 pathway in subarachnoid haemorrhage and its therapeutic potential
Neuroprotective role of Nrf2 pathway in subarachnoid haemorrhage and its therapeutic potential
The mechanisms underlying poor outcome following subarachnoid haemorrhage (SAH) are complex and multifactorial. They include early brain injury, spreading depolarisation, inflammation, oxidative stress, macroscopic cerebral vasospasm and microcirculatory disturbances. Nrf2 is a global promoter of the anti-oxidant and anti-inflammatory response and has potential protective effects against all of these mechanisms. It has been shown to be upregulated after SAH, and Nrf2 knockout animals have poorer functional and behavioural outcomes after SAH. There are many agents known to activate the Nrf2 pathway. Of these, the actions of sulforaphane, curcumin, astaxanthin, lycopene, tert-butyl hydroquinone, dimethyl fumarate, melatonin and erythropoietin have been studied in SAH models. This review details the different mechanisms of injury after SAH including the contribution of haemoglobin (Hb) and its breakdown products. It then summarises the evidence that the Nrf2 pathway is active and protective after SAH, and finally examines the evidence supporting Nrf2 upregulation as a therapy after SAH.
Zolnourian, Ardalan
5e8d4881-cdfd-4cb1-8eae-b98b13104648
Galea, Ian
66209a2f-f7e6-4d63-afe4-e9299f156f0b
Bulters, D.O.
a0586d7d-a447-464d-9ec6-fe151a22babe
Zolnourian, Ardalan
5e8d4881-cdfd-4cb1-8eae-b98b13104648
Galea, Ian
66209a2f-f7e6-4d63-afe4-e9299f156f0b
Bulters, D.O.
a0586d7d-a447-464d-9ec6-fe151a22babe
Zolnourian, Ardalan, Galea, Ian and Bulters, D.O.
(2019)
Neuroprotective role of Nrf2 pathway in subarachnoid haemorrhage and its therapeutic potential.
Oxidative Medicine and Cellular Longevity.
(In Press)
Abstract
The mechanisms underlying poor outcome following subarachnoid haemorrhage (SAH) are complex and multifactorial. They include early brain injury, spreading depolarisation, inflammation, oxidative stress, macroscopic cerebral vasospasm and microcirculatory disturbances. Nrf2 is a global promoter of the anti-oxidant and anti-inflammatory response and has potential protective effects against all of these mechanisms. It has been shown to be upregulated after SAH, and Nrf2 knockout animals have poorer functional and behavioural outcomes after SAH. There are many agents known to activate the Nrf2 pathway. Of these, the actions of sulforaphane, curcumin, astaxanthin, lycopene, tert-butyl hydroquinone, dimethyl fumarate, melatonin and erythropoietin have been studied in SAH models. This review details the different mechanisms of injury after SAH including the contribution of haemoglobin (Hb) and its breakdown products. It then summarises the evidence that the Nrf2 pathway is active and protective after SAH, and finally examines the evidence supporting Nrf2 upregulation as a therapy after SAH.
Text
Zolnourian et al 2019 postprint
- Accepted Manuscript
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Accepted/In Press date: 20 March 2019
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Local EPrints ID: 429310
URI: http://eprints.soton.ac.uk/id/eprint/429310
ISSN: 1942-0900
PURE UUID: 9db77f0e-8310-42d3-bf2a-4e7de035f69c
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Date deposited: 26 Mar 2019 17:30
Last modified: 16 Mar 2024 03:33
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Author:
Ardalan Zolnourian
Author:
D.O. Bulters
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