GPx-1-encoded adenoviral vector attenuates dopaminergic impairments induced by methamphetamine in GPx-1 knockout mice through modulation of NF-κB transcription factor

Sharma, Naveen; Shin, Eun Joo; Pham, Duc Toan; Sharma, Garima; Dang, Duy Khanh; Duong, Chu Xuan; Kang, Sang Won; Nah, Seung Yeol; Jang, Choon‐Gon; Lei, Xin Gen; Nabeshima, Toshitaka; Bing, Guoying; Jeong, Ji Hoon; Kim, Hyoung Chun

doi:10.1016/j.fct.2021.112313

Cited by 11 publications

(5 citation statements)

References 94 publications

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“…The transcription factor NF-κB plays a vital role in cellular death and survival under oxidative stress conditions ( Li and Karin, 1999 ), and the activation of NF-κB can promote cell death ( Schneider et al, 1999 ; Zhang et al, 2005 ). Recently, the correlation between GPX1 and NF-κB pathway has been declared ( Koeberle et al, 2020 ; Sharma et al, 2021b ). Therefore, to identify the role of NF-κB and the regulative mechanism between GPX1 and NF-κB in SGNs damage induced by peroxynitrite, we measured the NF-κB pathway in SGNs after peroxynitrite administration with GPX1 upregulation or deficiency ( Figure 8A ).…”

Section: Resultsmentioning

confidence: 99%

Glutathione Peroxidase 1 Protects Against Peroxynitrite-Induced Spiral Ganglion Neuron Damage Through Attenuating NF-κB Pathway Activation

Wang

Han

Chen

et al. 2022

Front. Cell. Neurosci.

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Glutathione peroxidase 1 (GPX1) is a crucial antioxidant enzyme that prevented the harmful accumulation of intra-cellular hydrogen peroxide. GPX1 might contribute in limiting cochlear damages associated with aging or acoustic overexposure, but the function of GPX1 in the inner ear remains unclear. The present study was designed to investigate the effect of GPX1 on cochlear spiral ganglion neurons (SGNs) against oxidative stress induced by peroxynitrite, a versatile oxidant generated by the reaction of superoxide anion and nitric oxide. Here, we first found that the expression of GPX1 in cultured SGNs was downregulated after peroxynitrite exposure. Then, the GPX1 mimic ebselen and the gpx1 knockout (gpx1–/–) mice were used to investigate the role of GPX1 in SGNs treated with peroxynitrite. The pretreatment with ebselen significantly increased the survived SGN numbers, inhibited the apoptosis, and enhanced the expression of 4-HNE in the cultured SGNs of peroxynitrite + ebselen group compared with the peroxynitrite-only group. On the contrary, remarkably less survived SGNs, more apoptotic SGNs, and the higher expression level of 4-HNE were detected in the peroxynitrite + gpx1–/– group compared with the peroxynitrite-only group. Furthermore, rescue experiments with antioxidant N-acetylcysteine (NAC) showed that the expression of 4-HNE and the apoptosis in SGNs were significantly decreased, while the number of surviving SGNs was increased in peroxynitrite + NAC group compared the peroxynitrite-only group and in peroxynitrite + gpx1–/– + NAC group vs. peroxynitrite + gpx1–/– group. Finally, mechanistic studies showed that the activation of nuclear factor-kappa B (NF-κB) was involved in the SGNs damage caused by peroxynitrite and that GPX1 protected SGNs against peroxynitrite-induced damage, at least in part, via blocking the NF-κB pathway activation. Collectively, our findings suggest that GPX1 might serve as a new target for the prevention of nitrogen radical-induced SGNs damage and hearing loss.

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Section: Resultsmentioning

confidence: 99%

Glutathione Peroxidase 1 Protects Against Peroxynitrite-Induced Spiral Ganglion Neuron Damage Through Attenuating NF-κB Pathway Activation

Wang

Han

Chen

et al. 2022

Front. Cell. Neurosci.

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“…This result is similar to the result obtained in our present study. Some of the Nrf2-regulated genes (such as HO-1 and GPX1) have binding sites for the oxidative stress-sensitive transcription factor nuclear factor-kappa-B (NF-κB) in their regulatory regions [43][44][45]. In this study, we investigated whether equal doses (50 mg/kg) of sulforaphane, curcumin, quercetin, BHA, and I3C induced the translocation of NF-κB into the nuclear fraction of the mouse liver with a similar pattern and intensity.…”

Section: Discussionmentioning

confidence: 99%

“…A large number of hepatoprotective reagents have been shown to activate the Nrf2-related gene expression and suppressed NF-κB expression [41]. Some phase II antioxidant genes possess binding sites for NF-κB in their regulatory element region [43][44][45]. With regard to these aspects, apart from Nrf2 nuclear translocation, we also investigated whether NF-κB is translocated into the liver nuclear fraction and affect the expression of our genes of interest.…”

Section: Introductionmentioning

confidence: 99%

Effect of Administration of an Equal Dose of Selected Dietary Chemicals on Nrf2 Nuclear Translocation in the Mouse Liver

Alrawaiq

Atia

Abdullah

2023

Oxidative Medicine and Cellular Longevity

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Certain dietary chemicals influenced the expression of chemopreventive genes through the Nrf2-Keap1 pathway. However, the difference in Nrf2 activation potency of these chemicals is not well studied. This study is aimed at determining the difference in the potency of liver Nrf2 nuclear translocation induced by the administration of equal doses of selected dietary chemicals in mice. Male ICR white mice were administered 50 mg/kg of sulforaphane, quercetin, curcumin, butylated hydroxyanisole, and indole-3-carbinol for 14 days. On day 15, the animals were sacrificed, and their livers were isolated. Liver nuclear extracts were prepared, and Nrf2 nuclear translocation was detected through Western blotting. To determine the implication of the Nrf2 nuclear translocation on the expression levels of several Nrf2-regulated genes, liver RNA was extracted for qPCR assay. Equal doses of sulforaphane, quercetin, curcumin, butylated hydroxyanisole, and indole-3-carbinol significantly induced the nuclear translocation of Nrf2 with different intensities and subsequently increased the expression of Nrf2-regulated genes with an almost similar pattern as the Nrf2 nuclear translocation intensities (sulforaphane > butylated hydroxyanisole = indole-3-carbinol > curcumin > quercetin). In conclusion, sulforaphane is the most potent dietary chemical that induces the Nrf2 translocation into the nuclear fraction in the mouse liver.

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“…Oxidative stress was involved in schizophrenia pathogenesis ( 11 , 34 ), and at least half of selenoproteins participate in suppressing oxidative stress ( 9 ). Dopamine has been proposed to contribute significantly to the pathophysiology of schizophrenia ( 35 ), and selenium-dependent glutathione peroxidase plays a protective role against dopaminergic toxicity induced by methamphetamine ( 36 ). Additionally, fatty acids reported to have a significantly negative association with selenium ( 10 ) were identified as a potential risk for schizophrenia ( 37 ).…”

Section: Discussionmentioning

confidence: 99%

Genetic association between circulating selenium level and the risk of schizophrenia in the European population: A two-sample Mendelian randomization study

Deng

Cui²,

Nie³

et al. 2022

Front. Nutr.

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BackgroundThe association between circulating the selenium level and the risk of schizophrenia remains unclear.ObjectiveTo determine the relationship between the circulating selenium level and the risk of schizophrenia, using the Mendelian Randomization method in the European population.MethodsSingle nucleotide polymorphisms (SNPs) associated with the circulating selenium level were identified at p < 5 × 10−8. The inverse variance weighted (IVW) method was used as the principal MR analysis, and MR Egger, weighted median, and MR PRESSO were used to determine the accuracy of IVW results. The Cochran's Q-test and Leave-One-Out sensitivity analysis were performed to evaluate the heterogeneity and stability of genetic variants on schizophrenia.ResultsThe circulating selenium level was associated with decreased risk of schizophrenia by the IVW method (OR: 0.906, 95% CI:0.867–0.947). MR Egger, weighted median, and MR PRESSO methods got similar results. No heterogeneity was detected by the Cochran's Q-test, and no single SNP was driving the overall effect by leave-one-out analysis.ConclusionOur study provides support for the genetic relationship between the circulating selenium level and schizophrenia; the decreased circulating selenium level was associated with an elevated risk of schizophrenia.

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GPx-1-encoded adenoviral vector attenuates dopaminergic impairments induced by methamphetamine in GPx-1 knockout mice through modulation of NF-κB transcription factor

Cited by 11 publications

References 94 publications

Glutathione Peroxidase 1 Protects Against Peroxynitrite-Induced Spiral Ganglion Neuron Damage Through Attenuating NF-κB Pathway Activation

Glutathione Peroxidase 1 Protects Against Peroxynitrite-Induced Spiral Ganglion Neuron Damage Through Attenuating NF-κB Pathway Activation

Effect of Administration of an Equal Dose of Selected Dietary Chemicals on Nrf2 Nuclear Translocation in the Mouse Liver

Genetic association between circulating selenium level and the risk of schizophrenia in the European population: A two-sample Mendelian randomization study

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