Sulforaphane alleviates ethanol-mediated central inhibition and reverses chronic stress-induced aggravation of acute alcoholism via targeting Nrf2-regulated catalase expression

Xu, Junfeng; Lu, Jia-Jing; Cao, Yu; Wang, Wen; Li, Hou-Hong; Chen, Jianguo; Wang, Fang; Wu, Pengfei

doi:10.1016/j.neuropharm.2020.108235

Cited by 7 publications

(3 citation statements)

References 60 publications

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“…Furthermore, SF administration reduced CPZ-induced oxidative stress in both cardiac and hepatic tissues. Our results run in accordance with Greco et al [ 86 ] and Xu et al [ 70 ] that showed that treatment of induced rats with SF increases Nrf-2-mediated antioxidant defenses; this might be explained by the ability of SF as Nrf2 regulator to control CPZ intoxication, possibly by potentiating catalase function, signifying that the re-activation of the “Nrf2-catalase signaling pathway” and enhancing the “peroxidase activity” of catalase. SF demonstrated anti-inflammatory and anti-oxidative activities as demonstrated previously [ 87 – 89 ].…”

Section: Discussionsupporting

confidence: 93%

“…Moreover, the translocation of Nrf-2 to the nucleus enables its interaction with the antioxidant response element (ARE) to boost the cytoprotective “anti-oxidative” gene expression, such as HO-1 and NAD(P)H: quinone oxidoreductase 1 (NQO1), to produce catalase to exert anti-oxidative function [ 69 ]. Herein, we estimated the catalase activities and evaluated the immunostaining % of Nrf-2; as Nrf-2 controls the expression of antioxidant catalase, which is significantly influenced by redox status, as evidenced previously [ 70 ], although other antioxidant enzymes might be involved.…”

Section: Discussionmentioning

confidence: 99%

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Sulforaphane, an Nrf-2 Agonist, Modulates Oxidative Stress and Inflammation in a Rat Model of Cuprizone-Induced Cardiotoxicity and Hepatotoxicity

Fouad

2023

Cardiovasc Toxicol

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Cuprizone (CPZ) is a neurotoxic agent that is used to induce demyelination and neurotoxicity in rats. This study aimed to investigate the protective potential of sulforaphane (SF), nuclear factor E2 related factor (Nrf-2) activator, against CPZ-induced cardiotoxicity and hepatotoxicity. Male adult Wistar rats (n = 18) were fed with a regular diet or a CPZ-contained diet (0.2%) for four weeks. The rats were divided into three groups (n = 6): negative control rats, CPZ-exposed rats, and CPZ + SF treated rats. SF was intraperitoneally administrated (2 mg/kg/day) for two weeks. The anti-inflammatory and anti-oxidative functions of SF were investigated biochemically, histologically, and immunohistochemically. CPZ increased serum levels of cardiac troponin 1 (CTn1), aspartate amino transaminase (AST), alanine amino transaminase (ALT), and alkaline phosphatase (ALP). In addition, serum levels of inflammatory interferon-gamma (IFN-γ), and pro-inflammatory interleukin 1β (IL-1β) were significantly elevated. Moreover, CPZ administration provoked oxidative stress as manifested by declined serum levels of total antioxidant capacity (TAC), as well as, stimulated lipid peroxidation and decreased catalase activities in both cardiac and hepatic tissues. SF treatment reversed all these biochemical alterations through exerting anti-oxidative and anti-inflammatory activities, and this was supported by histopathological investigations in both cardiac and hepatic tissues. This SF-triggered modulation of oxidative stress and inflammation is strongly associated with Nrf-2 activation, as evidenced by activated immunoexpression in both cardiac and hepatic tissues. This highlights the cardioprotective and hepatoprotective activities of SF via Nrf-2 activation and enhancing catalase function.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Sulforaphane, an Nrf-2 Agonist, Modulates Oxidative Stress and Inflammation in a Rat Model of Cuprizone-Induced Cardiotoxicity and Hepatotoxicity

Fouad

2023

Cardiovasc Toxicol

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“…On the other hand, several Nrf2-downstream proteins can mediate redox balance by neutralizing IR-derived ROS, such as superoxide anion and hydrogen peroxide. Particularly, superoxide dismutase and catalase, which metabolize superoxide anion and hydrogen peroxide, respectively, represent well-known Nrf2-downstream proteins [ 84 , 85 , 86 , 87 ]. Additional proteins, such as glutamate-cysteine ligase, glutathione peroxidase, glutathione reductase, thioredoxin reductase, heme oxygenase-1 and NADPH:quinone oxidoreductase, among others, are also known Nrf2-downstream molecules mediating redox balance and mitigating oxidative stress [ 74 ].…”

Section: Nrf2 Signaling Pathway and Ischemic Strokementioning

confidence: 99%

The Nrf2 Pathway in Ischemic Stroke: A Review

Farina

Vieira

Buttari³

et al. 2021

Molecules

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Ischemic stroke, characterized by the sudden loss of blood flow in specific area(s) of the brain, is the leading cause of permanent disability and is among the leading causes of death worldwide. The only approved pharmacological treatment for acute ischemic stroke (intravenous thrombolysis with recombinant tissue plasminogen activator) has significant clinical limitations and does not consider the complex set of events taking place after the onset of ischemic stroke (ischemic cascade), which is characterized by significant pro-oxidative events. The transcription factor Nuclear factor erythroid 2-related factor 2 (Nrf2), which regulates the expression of a great number of antioxidant and/or defense proteins, has been pointed as a potential pharmacological target involved in the mitigation of deleterious oxidative events taking place at the ischemic cascade. This review summarizes studies concerning the protective role of Nrf2 in experimental models of ischemic stroke, emphasizing molecular events resulting from ischemic stroke that are, in parallel, modulated by Nrf2. Considering the acute nature of ischemic stroke, we discuss the challenges in using a putative pharmacological strategy (Nrf2 activator) that relies upon transcription, translation and metabolically active cells in treating ischemic stroke patients.

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The NRF2 activator RTA-408 ameliorates chronic alcohol exposure-induced cognitive impairment and NLRP3 inflammasome activation by modulating impaired mitophagy initiation

Lin,

Wang,

Zou

et al. 2024

Free Radical Biology and Medicine

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Sulforaphane alleviates ethanol-mediated central inhibition and reverses chronic stress-induced aggravation of acute alcoholism via targeting Nrf2-regulated catalase expression

Cited by 7 publications

References 60 publications

Sulforaphane, an Nrf-2 Agonist, Modulates Oxidative Stress and Inflammation in a Rat Model of Cuprizone-Induced Cardiotoxicity and Hepatotoxicity

Sulforaphane, an Nrf-2 Agonist, Modulates Oxidative Stress and Inflammation in a Rat Model of Cuprizone-Induced Cardiotoxicity and Hepatotoxicity

The Nrf2 Pathway in Ischemic Stroke: A Review

The NRF2 activator RTA-408 ameliorates chronic alcohol exposure-induced cognitive impairment and NLRP3 inflammasome activation by modulating impaired mitophagy initiation

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