Nrf2/antioxidant defense pathway is involved in the neuroprotective effects of Sirt1 against focal cerebral ischemia in rats after hyperbaric oxygen preconditioning

Xue, Fen; Huang, Jinwen; Ding, Philip Yu‐An; Zang, Hong-gang; Kou, Zhijian; Li, Ting; Fan, Juan; Peng, Zhengwu; Yan, Wenjun

doi:10.1016/j.bbr.2016.04.045

Cited by 113 publications

(80 citation statements)

References 61 publications

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“…It regulates the transcription of a number of downstream genes through NAD + to participate in various cellular processes such as apoptosis, cell cycle, cell energy metabolism, oxidative stress, and cell aging process and is involved in a number of diseases such as diabetes, tumor, inflammation, aging, and neural degenerative diseases [8–10]. Earlier studies have revealed that the upregulation of Sirt1 activity or use of Sirt1 agonist resveratrol attenuates neurological injury in rats after cerebral ischemia through increased antioxidant capacity and neuronal survival although the mechanisms are largely unknown [11–15]. Also, it is not clear if rehabilitation training and Sirt1 agonist resveratrol have synergy in the recovery of motor functions after cerebral ischemia.…”

Section: Discussionmentioning

confidence: 99%

“…Studies have shown that Sirt1 is not only associated with inflammation, osteoarthritis, diabetes, cardiovascular disease, and cancer, but also associated with the progression of neurodegenerative diseases [8–10]. A large number of studies have shown that Sirt1 or its agonist resveratrol has a significant protective effect on neurons in rats after middle cerebral artery occlusion (MCAO) [11–15]. In addition, antioxidant transcription factor Nrf2 is also activated by resveratrol to upregulate the target genes such as NAD(P)H:quinone oxidoreductase 1, γ -glutamylcysteine synthetase, and heme oxygenase-1 to protect endothelial cells [16].…”

Section: Introductionmentioning

confidence: 99%

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Rehabilitation Training and Resveratrol Improve the Recovery of Neurological and Motor Function in Rats after Cerebral Ischemic Injury through the Sirt1 Signaling Pathway

Shi

Zhu

2016

BioMed Research International

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This study was conducted to investigate the recovery of motor function in rats through the silent information regulator factor 2-related enzyme 1 (Sirt1) signal pathway-mediated rehabilitation training. Middle cerebral artery occlusion (MACO) was used to induce ischemia/reperfusion injury. The rats were subjected to no treatment (model), rehabilitation training (for 21 days), resveratrol (5 mg/kg for 21 days), and rehabilitation training plus resveratrol treatment. 24 h later, They were assessed for neurobehavioral score and motor behavior score and expression of brain derived-nerve neurotrophic factor (BDNF) and tyrosine kinase receptor B (TrkB). Compared with sham group, models had significantly higher neurobehavioral scores, balance beam, and rotary stick scores. Compared with the model group, rats in rehabilitation training and resveratrol groups had significantly reduced scores. Compared with rehabilitation training or resveratrol treatment alone, rehabilitation plus resveratrol further reduced the scores significantly. The percentage of cells expressing BDNF and TrkB and expression levels of BDNF and TrkB were similar between the model and sham groups, significantly increased in rehabilitation training and resveratrol groups, and further increased in rehabilitation training plus resveratrol group. These results indicate that rehabilitation raining plus resveratrol can significantly improve the recovery of motor function in rats after cerebral ischemic injury, which is likely related to the upregulation of the BDNF/TrkB signaling pathway.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Rehabilitation Training and Resveratrol Improve the Recovery of Neurological and Motor Function in Rats after Cerebral Ischemic Injury through the Sirt1 Signaling Pathway

Shi

Zhu

2016

BioMed Research International

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“…The transfection of Nrf2 siRNA for rat brains in vivo were conducted according to the method described formerly [17, 31, 32]. Briefly, the rats were placed under anesthesia, then a cranial burr hole (1 mm in diameter) was drilled, following a 25-μl microsyringe with a needle tip (Shanghai high pigeon industry & trade co., LTD, Shanghai, China) was inserted stereotaxically into the right lateral ventricle.…”

Section: Methodsmentioning

confidence: 99%

Isoliquiritigenin alleviates early brain injury after experimental intracerebral hemorrhage via suppressing ROS- and/or NF-κB-mediated NLRP3 inflammasome activation by promoting Nrf2 antioxidant pathway

Zeng

Chen

Ding

et al. 2017

J Neuroinflammation

292

214

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BackgroundIntracerebral hemorrhage (ICH) induces potently oxidative stress responses and inflammatory processes. Isoliquiritigenin (ILG) is a flavonoid with a chalcone structure and can activate nuclear factor erythroid-2 related factor 2 (Nrf2)-mediated antioxidant system, negatively regulate nuclear factor-κB (NF-κB) and nod-like receptor family, pyrin domain-containing 3 (NLRP3) inflammasome pathways, but its role and potential molecular mechanisms in the pathology following ICH remain unclear. The present study aimed to explore the effects of ILG after ICH and underlying mechanisms.MethodsICH model was induced by collagenase IV (0.2 U in 1 μl sterile normal saline) in male Sprague-Dawley rats weighing 280–320 g. Different doses of ILG (10, 20, or 40 mg/kg) was administrated intraperitoneally at 30 min, 12 h, 24 h, and 48 h after modeling, respectively. Rats were intracerebroventricularly administrated with control scramble small interfering RNA (siRNA) or Nrf2 siRNA at 24 h before ICH induction, and after 24 h, ICH model was established with or without ILG (20 mg/kg) treatment. All rats were dedicated at 24 or 72 h after ICH. Neurological deficits, histological damages, brain water content (BWC), blood-brain barrier (BBB) disruption, and neuronal degeneration were evaluated; quantitative real-time RT-PCR (qRT-PCR), immunohistochemistry/immunofluorescence, western blot, and enzyme-linked immunosorbent assay (ELISA) were carried out; catalase, superoxide dismutase activities and reactive oxygen species (ROS), and glutathione/oxidized glutathione contents were measured.ResultsILG (20 and 40 mg/kg) markedly alleviated neurological deficits, histological damages, BBB disruption, brain edema, and neuronal degeneration, but there was no significant difference between two dosages. ILG (20 mg/kg) significantly suppressed the NF-κB and NLRP3 inflammasome pathways and activated Nrf2-mediated antioxidant system. Gene silencing of Nrf2 aggravated the neurological deficits, brain edema, and neuronal degeneration and increased the protein levels of NF-κB p65, NLRP3 inflammasome components, and IL-1β. ILG delivery significantly attenuated the effects of Nrf2 siRNA interference mentioned above.ConclusionsIntraperitoneal administration of ILG after ICH reduced early brain impairments and neurological deficits, and the mechanisms were involved in the regulation of ROS and/or NF-κB on the activation of NLRP3 inflammasome pathway by the triggering of Nrf2 activity and Nrf2-induced antioxidant system. In addition, our experimental results may make ILG a potential candidate for a novel therapeutical strategy for ICH.Electronic supplementary materialThe online version of this article (doi:10.1186/s12974-017-0895-5) contains supplementary material, which is available to authorized users.

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“…Furthermore, through regulating the Nrf2 deacetylation function, SIRT1 can improve Nrf2 stability. Therefore, SIRT1 could help cells to avoid oxidative stress-induced injury through active Nrf2 and its downstream gene expressions (Xue et al, 2016). …”

Section: Introductionmentioning

confidence: 99%

SRT1720 Alleviates ANIT-Induced Cholestasis in a Mouse Model

Liu

Yuan

et al. 2017

Front. Pharmacol.

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Intrahepatic cholestasis is a kind of clinical syndrome along with hepatotoxicity which caused by intrahepatic and systemic accumulations of bile acid. There are several crucial generating factors of the pathogenesis of cholestasis, such as inflammation, dysregulation of bile acid transporters and oxidative stress. SIRT1 is regarded as a class III histone deacetylase (HDAC). According to a set of researches, SIRT1 is one of the most important factors which can regulate the hepatic bile acid metabolism. SRT1720 is a kind of activator of SIRT1 which is 1000 times more potent than resveratrol, and this paper is aimed to study its protective influence on hepatotoxicity and cholestasis induced by alpha-naphthylisothiocyanate (ANIT) in mice. The findings revealed that SRT1720 treatment increased FXR and Nrf2 gene expressions to shield against hepatotoxicity and cholestasis induced by ANIT. The mRNA levels of hepatic bile acid transporters were also altered by SRT1720. Furthermore, SRT1720 enhanced the antioxidative system by increasing Nrf2, SOD, GCLc, GCLm, Nqo1, and HO-1 gene expressions. In conclusion, a protective influence could be provided by SRT1720 to cure ANIT-induced hepatotoxicity and cholestasis, which was partly through FXR and Nrf2 activations. These results indicated that SIRT1 could be regarded as a therapeutic target to cure the cholestasis.

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Nrf2/antioxidant defense pathway is involved in the neuroprotective effects of Sirt1 against focal cerebral ischemia in rats after hyperbaric oxygen preconditioning

Cited by 113 publications

References 61 publications

Rehabilitation Training and Resveratrol Improve the Recovery of Neurological and Motor Function in Rats after Cerebral Ischemic Injury through the Sirt1 Signaling Pathway

Rehabilitation Training and Resveratrol Improve the Recovery of Neurological and Motor Function in Rats after Cerebral Ischemic Injury through the Sirt1 Signaling Pathway

Isoliquiritigenin alleviates early brain injury after experimental intracerebral hemorrhage via suppressing ROS- and/or NF-κB-mediated NLRP3 inflammasome activation by promoting Nrf2 antioxidant pathway

SRT1720 Alleviates ANIT-Induced Cholestasis in a Mouse Model

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