Expression and antioxidation of Nrf2/ARE pathway in traumatic brain injury

Cheng, Zhenguo; Zhang, Guodong; Shi, Pengqiang; Du, Botao

doi:10.1016/s1995-7645(13)60061-9

Cited by 30 publications

(25 citation statements)

References 20 publications

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“…These antioxidant and detoxifying factors encompass many important protective mechanisms for secondary brain injury following traumatic brain injury (Miller et al, 2014;Sandberg et al, 2014). Previous studies have found that expression of Nrf2 begins to increase 2 h after traumatic brain injury, and its expression peaks after 24 h. Nrf2 expression then gradually decreases and returns to normal levels 3 to 5 days later (Cheng et al, 2013). The degree of traumatic brain injury in Nrf2 knockout mice is significantly more severe compared to wild type mice, and administration of drugs that up-regulate Nrf2 protein expression significantly reduces apoptosis of neurons and improves neurological function after traumatic brain injury Xie et al, 2014;Xu et al, 2014).…”

Section: Discussionmentioning

confidence: 99%

Effects of hyperbaric oxygen on the Nrf2 signaling pathway in secondary injury following traumatic brain injury

Meng¹,

Zhang²,

Li³

et al. 2016

Genet. Mol. Res.

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ABSTRACT. We investigated the effects of hyperbaric oxygen treatment on the Nrf2 signaling pathway in secondary injury following traumatic brain injury, using a rat model. An improved Feeney freefall method was used to establish the rat traumatic brain injury model. Sixty rats were randomly divided into three groups: a sham surgery group, a traumatic brain injury group, and a group receiving hyperbaric oxygen treatment after traumatic brain injury. Neurological function scores were assessed at 12 and 24 h after injury. The expression levels of Nrf2, heme oxygenase 1 (HO-1), and quinine oxidoreductase 1 (NQO-1) in the cortex surrounding the brain lesion were detected by western blotting 24 h after the injury. Additionally, the TUNEL method was used to detect apoptosis of nerve cells 24 h after traumatic injury and Nissl staining was used to detect the number of whole neurons. Hyperbaric oxygen treatment significantly increased the expression of nuclear Nrf2 protein (P < 0.05), HO-1, and NQO-1 in the brain tissues surrounding the lesion after a traumatic brain injury (P < 0.05) and also significantly reduced the number of apoptotic and injured nerve cells. The neurological function scores also improved with hyperbaric oxygen treatment (P < 0.05). Therefore, hyperbaric oxygen has a neuroprotective role in traumatic brain injury, which is mediated by up-regulation of the Nrf2 signaling pathway.

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Section: Discussionmentioning

confidence: 99%

Effects of hyperbaric oxygen on the Nrf2 signaling pathway in secondary injury following traumatic brain injury

Meng¹,

Zhang²,

Li³

et al. 2016

Genet. Mol. Res.

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“…When oxidative stress stimulus occurs, it is decoupled with Keapl through phosphorylation, transfers into nucleus, combines with antioxidant response element (ARE) sequence, forms Nrf2/ARE pathway and then starts the gene expression of phase II detoxifying enzymes and antioxidases (H0-1, NQO1, etc) regulated by ARE. Nrf2/ARE pathway plays an important role in endogenous anti-oxidation process in vivo and can be induced by external factors (14).…”

Section: Neuroprotection and Emerging Roles Of Nrf2mentioning

confidence: 99%

“…These evidences demonstrate that activation of the Nrf2-ARE pathway is beneficial for TBI. (16) It is now accepted that the Nrf2-ARE pathway can be regulated in many different ways (14,16,36).…”

Section: Neuroprotection and Emerging Roles Of Nrf2mentioning

confidence: 99%

“…Various mechanisms are postulated to promote free radical production, including glutamate release, intracelular calcium overload, increase in arachidonic acid and its metabolites, hemoglobin denaturation, and iron ion release (1). The production of free radicals evoked by brain injury plays a crucial role in the initiating and propagating the pathogenesis of post-traumatic secondary injury, through oxidation and nitration of the cellular membrane, proteins, and DNA (3,(13)(14)(15)(16).…”

Section: Introductionmentioning

confidence: 99%

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Antioxidant therapies in traumatic brain injury: a review

Romero-Rivera¹,

Cabeza-Morales²,

Soto-Zarate³

et al. 2017

Romanian Neurosurgery

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Abstract:Oxidative stress constitute one of the commonest mechanism of the secondary injury contributing to neuronal death in traumatic brain injury cases. The oxidative stress induced secondary injury blockade may be considered as to be a good alternative to improve the outcome of traumatic brain injury (TBI) treatment. Due to absence of definitive therapy of traumatic brain injury has forced researcher to utilize unconventional therapies and its roles investigated in the improvement of management and outcome in recent year. Antioxidant therapies are proven effective in many preclinical studies and encouraging results and the role of antioxidant mediaction may act as further advancement in the traumatic brain injury management it may represent aonr of newer moadlaity in neurosurgical aramamentorium, this kind of therapy could be a good alternative or adjuct to the previously established neuroprotection agents in TBI.

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“…The nuclear factor (erythroid-derived 2)-like 2 (NFE2L2 or Nrf2) signaling pathway regulates the level of expression of antioxidant proteins that protect against oxidative injury induced by trauma and inflammation, and this pathway has increasingly attracted attention in studies of the molecular mechanism of ROS in TBI (57). In rat and mouse experiments, activation of the Nrf2 pathway has been found to inhibit ROS-induced damage in brain tissue (58).…”

Section: Clinical Treatmentmentioning

confidence: 99%