Activation of Nrf2-ARE signal pathway in hippocampus of amygdala kindling rats

Wang, Wei; Wang, Weiping; Zhang, Guoliang; Wu, Yanfen; Xie, Ting; Kan, Min-chen; Fang, Haibo; Wang, Hong-chao

doi:10.1016/j.neulet.2013.03.038

Cited by 39 publications

(44 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The transient activation of Nrf2-ARE pathway might be a response to the oxidative stress caused by SE [55], but SE-induced Nrf2 activation was not enough to protect neurons from oxidative damage, which underlay the defects in mesodopaminergic system, as well as the elevated LPO and MDA in SN-VTA and Hip of SE rats in the present studies. However, Nrf2-ARE pathway provides a potential target in controlling epileptic seizures [24, 55]. …”

Section: Discussionmentioning

confidence: 70%

“…When Nrf2 is activated, it is translocated into the nucleus and combined with the ARE to induce a series of cytoprotective enzymes such as HO-1 [49, 50] and NQO-1 [51, 52] to enhance the antioxidant capacity of cells and protect cells from the oxidative injury [53, 54]. In the present studies, the elevation of Nrf2, HO-1, and NQO-1 at mRNA and protein levels found in SE rats 24 hrs but not 7 days following Li-Pc injection indicated that epileptic seizures could transiently activate Nrf2-ARE pathway [55]. The transient activation of Nrf2-ARE pathway might be a response to the oxidative stress caused by SE [55], but SE-induced Nrf2 activation was not enough to protect neurons from oxidative damage, which underlay the defects in mesodopaminergic system, as well as the elevated LPO and MDA in SN-VTA and Hip of SE rats in the present studies.…”

Section: Discussionmentioning

confidence: 72%

“…In the present studies, the elevation of Nrf2, HO-1, and NQO-1 at mRNA and protein levels found in SE rats 24 hrs but not 7 days following Li-Pc injection indicated that epileptic seizures could transiently activate Nrf2-ARE pathway [55]. The transient activation of Nrf2-ARE pathway might be a response to the oxidative stress caused by SE [55], but SE-induced Nrf2 activation was not enough to protect neurons from oxidative damage, which underlay the defects in mesodopaminergic system, as well as the elevated LPO and MDA in SN-VTA and Hip of SE rats in the present studies. However, Nrf2-ARE pathway provides a potential target in controlling epileptic seizures [24, 55].…”

Section: Discussionmentioning

confidence: 77%

See 2 more Smart Citations

Alleviation of Oxidative Damage and Involvement of Nrf2‐ARE Pathway in Mesodopaminergic System and Hippocampus of Status Epilepticus Rats Pretreated by Intranasal Pentoxifylline

Kang

Yan

Fang

et al. 2017

Oxidative Medicine and Cellular Longevity

View full text Add to dashboard Cite

The current studies were aimed at evaluating the efficacy of intranasal pentoxifylline (Ptx) pretreatment in protecting mesodopaminergic system and hippocampus from oxidative damage of lithium-pilocarpine induced status epilepticus (SE) and the involvement of nuclear factor erythroid 2-related factor 2- (Nrf2-) antioxidant response elements pathway. Pentoxifylline was administered to rats intranasally or intraperitoneally 30 minutes before inducing SE. Our results showed the impaired visuospatial memory, the defected mesodopaminergic system, and the oxidative damage and the transient activation of Nrf2 in SE rats. The transient activation of Nrf2 in SE rats was enhanced by Ptx pretreatment, which was followed by the upregulation of heme oxygenase-1 and NAD(P)H:quinone oxidoreductase-1. Ptx pretreatment to SE rats significantly suppressed the epileptic seizures, decreased the levels of lipid peroxide and malondialdehyde, and elevated the ratio of reduced glutathione/oxidized glutathione. Compared with intraperitoneal injection, intranasal Ptx delivery completely restored the visuospatial memory and the activity of mesodopaminergic system in SE rats. Intranasal administration of Ptx may hopefully become a noninvasive, painless, and easily administered option for epileptic patients.

show abstract

Section: Discussionmentioning

confidence: 70%

Section: Discussionmentioning

confidence: 72%

Section: Discussionmentioning

confidence: 77%

See 1 more Smart Citation

Alleviation of Oxidative Damage and Involvement of Nrf2‐ARE Pathway in Mesodopaminergic System and Hippocampus of Status Epilepticus Rats Pretreated by Intranasal Pentoxifylline

Kang

Yan

Fang

et al. 2017

Oxidative Medicine and Cellular Longevity

View full text Add to dashboard Cite

show abstract

“…Previous studies have demonstrated that the expression of Nrf2 and HO-1 at protein and mRNA levels markedly increased in hippocampus of amygdala kindling rats [55, 56]. Moreover, activation of Nrf2-ARE signal pathway in hippocampus reduced the progression of amygdale kindling, and alleviated the cognitive impairment and oxidative stress induced by epileptic seizure [21, 57].…”

Section: Discussionmentioning

confidence: 99%

Ginsenoside Rb1 Protects the Brain from Damage Induced by Epileptic Seizure via Nrf2/ARE Signaling

Shi

Wang

Teng

et al. 2018

Cell Physiol Biochem

View full text Add to dashboard Cite

Background/Aims: Ginsenoside Rb1 (Rb1) has been reported to have varieties of neuroprotective effects. This study aimed to evaluate the effects of Rb1 on pentylenetetrazol (PTZ)-induced rat brain injury and Mg²⁺ free-induced neuron injury and analyzed the detailed molecular mechanisms in vivo and in vitro. Methods: Seizure duration and latency were measured in epilepsy kindled rat. The cognitive impairment was assessed by Morris water maze (MWM) test. Oxidative stress parameters, malondialdehyde (MDA) and glutathione (GSH) were measured by the 2-thiobarbituric acid methods and the DTNB-GSSG reductase recycling methods. Neuronal damage was assessed by hematoxylin and eosin (H&E) and Nissl staining. Neuronal apoptosis was measured by Annexin V-FITC and propidium iodide (PI) staining. Immunohistochemistry and immunofluorescence staining were performed to evaluate Nrf2 and HO-1 expressions. Expression of Nrf2, HO-1, Bcl-2, iNOS and LC3 were evaluated by western blot. Results: The PTZ-injured rats presented longer seizure duration and shorter seizure latency. Rb1 ameliorated these effects, as well as the cognitive deficits caused by PTZ exposure. Besides, Rb1 dose-dependently increased GSH levels, decreased MDA levels and alleviated neuronal damage in PTZ-treated rats. In vitro, Rb1 increased cell viability and decreased neuronal apoptosis in a dose-dependent manner under Mg²⁺ free condition. Moreover, in vivo and in vitro, Rb1 enhanced both the Nrf2 and HO-1 expressions. Furthermore, upregulation of the expression of Bcl-2 and downregulation of the expression of iNOS and LC3 were observed. However, knockdown of Nrf2 adversely affected the protective effects of Rb1 in epileptic hippocampal neurons. Conclusion: Rb1 conferred neuroprotective effects against PTZ-induced brain damage and Mg²⁺ free-induced neuron injury by activating Nrf2/ARE signaling.

show abstract

“…We speculate that TQ alleviates the brain injury of SE by modulating oxidative stress. It is thought that the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway plays a key defensive role against oxidative stress in epilepsy [12–14]. This study evaluated the protective effects of TQ on brain injury in a status epilepticus rat model, and the underlying mechanism related to antioxidative pathway using biochemistry techniques and behavioral and electrophysiological tests.…”

Section: Introductionmentioning

confidence: 99%

Thymoquinone attenuates brain injury via an antioxidative pathway in a status epilepticus rat model

Shao

Huang

et al. 2017

Translational Neuroscience

View full text Add to dashboard Cite

Status epilepticus (SE) is a common, lifethreatening neurologic disorder characterized by acute, prolonged epileptic seizures. The incidence rate of SE is about 0.05 to 0.1% in the general population and 1.1 to 14% in the epileptic population. SE has a poor prognosis because seizures that cannot be terminated quickly result in irreversible brain injury. It is known that multiple factors are involved in the pathogenesis of brain injury induced by SE, one of which is oxidative stress [1][2]. The generation of excess free radicals and increase in lipid peroxidation that occur during SE damage brain tissue, therefore, antioxidants might be effective for treatment of SE [3][4][5].Thymoquinone (TQ), a bioactive monomer derived from black seed (Nigella sativa) oil, has significant antioxidant effects [6][7][8]. It has been shown to suppress oxidative stress and attenuate seizure activity and lower hippocampal neuronal loss in an epilepsy model and in children with refractory seizures [9][10][11]. We speculate that TQ alleviates the brain injury of SE by modulating oxidative stress. It is thought that the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway plays a key defensive role against oxidative stress in epilepsy [12][13][14]. This study evaluated the protective effects of TQ on brain injury in a status epilepticus rat model, and the underlying mechanism related to antioxidative pathway using biochemistry techniques and behavioral and electrophysiological tests. Materials and methods THYMOQUINONE ATTENUATES BRAIN INJURY VIA AN ANTI-OXIDATIVE PATHWAY IN A STATUS EPILEPTICUS RAT MODEL AbstractAim: Status epilepticus (SE) results in the generation of reactive oxygen species (ROS), which contribute to seizure-induced brain injury. It is well known that oxidative stress plays a pivotal role in status epilepticus (SE). Thymoquinone (TQ) is a bioactive monomer extracted from black cumin (Nigella sativa) seed oil that has anti-inflammatory, anti-cancer, and antioxidant activity in various diseases. This study evaluated the protective effects of TQ on brain injury in a lithium-pilocarpine rat model of SE and investigated the underlying mechanism related to antioxidative pathway. Methods: Electroencephalogram and Racine scale were used to value seizure severity. Passive-avoidance test was used to determine learning and memory function. Moreover, anti-oxidative activity of TQ was observed using Western blot and super oxide dismutase (SOD) activity assay. Results: Latency to SE increased in the TQ-pretreated group compared with rats in the model group, while the total power was significantly lower. Seizure severity measured on the Racine scale was significantly lower in the TQ group compared with the model group. Results of behavioral experiments suggest that TQ may also have a protective effect on learning and memory function. Investigation of the protective mechanism of TQ showed that TQ-pretreatment significantly increased the expression of Nrf2, HO-1 proteins and SOD in the hippocampus. Conclusion: these findings...

show abstract

Activation of Nrf2-ARE signal pathway in hippocampus of amygdala kindling rats

Cited by 39 publications

References 27 publications

Alleviation of Oxidative Damage and Involvement of Nrf2‐ARE Pathway in Mesodopaminergic System and Hippocampus of Status Epilepticus Rats Pretreated by Intranasal Pentoxifylline

Alleviation of Oxidative Damage and Involvement of Nrf2‐ARE Pathway in Mesodopaminergic System and Hippocampus of Status Epilepticus Rats Pretreated by Intranasal Pentoxifylline

Ginsenoside Rb1 Protects the Brain from Damage Induced by Epileptic Seizure via Nrf2/ARE Signaling

Thymoquinone attenuates brain injury via an antioxidative pathway in a status epilepticus rat model

Contact Info

Product

Resources

About