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Pesquisa : G02.111.570.080.689.675.700.040 [Categoria DeCS]
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[PMID]:28986252
[Au] Autor:Huang TT; Hao DL; Wu BN; Mao LL; Zhang J
[Ad] Endereço:Department of Neurology, Wujin Hospital Affiliated to Jiangsu University, Changzhou 213002, Jiangsu, China.
[Ti] Título:Uric acid demonstrates neuroprotective effect on Parkinson's disease mice through Nrf2-ARE signaling pathway.
[So] Source:Biochem Biophys Res Commun;493(4):1443-1449, 2017 Dec 02.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Uric acid has neuroprotective effect on Parkinson's disease (PD) by inhibiting oxidative damage and neuronal cell death. Our previous study has shown that uric acid protected dopaminergic cell line damage through inhibiting accumulation of NF-E2-related factor 2 (Nrf2). This study aimed to investigate its in vivo neuroprotective effect. PD was induced by MPTP intraperitoneally injection for 7 d in male C57BL/6 mice. Mice were treated with either uric acid (intraperitoneally injection 250 mg/kg) or saline for a total of 13 d. We showed that uric acid improved behavioral performances and cognition of PD mice, increased TH-positive dopaminergic neurons and decreased GFAP-positive astrocytes in substantia nigra (SN). Uric acid increased mRNA and protein expressions of Nrf2 and three Nrf2-responsive genes, including γ-glutamate-cysteine ligase catalytic subunit (γ-GCLC), heme oxygenase-1 (HO-1) and NQO1. Uric acid significantly increased superoxide dismutase (SOD), CAT, glutathione (GSH) levels and decreased malondialdehyde (MDA) level in SN regions of MPTP-treated mice. Uric acid inhibited the hippocampal expression of IL-1ß and decreased serum and hippocampus levels of interleukin-1ß (IL-1ß), IL-6 and tumor necrosis factor-α (TNF-α). In conclusion, uric acid demonstrates neuroprotective properties for dopaminergic neurons in PD mice through modulation of neuroinflammation and oxidative stress.
[Mh] Termos MeSH primário: Elementos de Resposta Antioxidante/efeitos dos fármacos
Fator 2 Relacionado a NF-E2/metabolismo
Fármacos Neuroprotetores/farmacologia
Doença de Parkinson/tratamento farmacológico
Doença de Parkinson/fisiopatologia
Ácido Úrico/farmacologia
[Mh] Termos MeSH secundário: Animais
Comportamento Animal/efeitos dos fármacos
Cognição/efeitos dos fármacos
Citocinas/sangue
Citocinas/metabolismo
Hipocampo/efeitos dos fármacos
Hipocampo/patologia
Hipocampo/fisiopatologia
Inflamação/tratamento farmacológico
Inflamação/patologia
Intoxicação por MPTP/tratamento farmacológico
Intoxicação por MPTP/fisiopatologia
Intoxicação por MPTP/psicologia
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Estresse Oxidativo/efeitos dos fármacos
Doença de Parkinson/psicologia
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (NF-E2-Related Factor 2); 0 (Neuroprotective Agents); 0 (Nfe2l2 protein, mouse); 268B43MJ25 (Uric Acid)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171008
[St] Status:MEDLINE


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[PMID]:28928081
[Au] Autor:Liao W; Fu Z; Zou Y; Wen D; Ma H; Zhou F; Chen Y; Zhang M; Zhang W
[Ad] Endereço:Department of Nephrology, Ruijin Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China.
[Ti] Título:MicroRNA-140-5p attenuated oxidative stress in Cisplatin induced acute kidney injury by activating Nrf2/ARE pathway through a Keap1-independent mechanism.
[So] Source:Exp Cell Res;360(2):292-302, 2017 Nov 15.
[Is] ISSN:1090-2422
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Oxidative stress was predominantly involved in the pathogenesis of acute kidney injury (AKI). Recent studies had reported the protective role of specific microRNAs (miRNAs) against oxidative stress. Hence, we investigated the levels of miR140-5p and its functional role in the pathogenesis of Cisplatin induced AKI. A mice Cisplatin induced-AKI model was established. We found that miR-140-5p expression was markedly increased in mice kidney. Bioinformatics analysis revealed nuclear factor erythroid 2-related factor (Nrf2) was a potential target of miR-140-5p, We demonstrated that miR-140-5p did not affect Kelch-like ECH-associated protein 1 (Keap1) level but directly targeted the 3'-UTR of Nrf2 mRNA and played a positive role in the regulation of Nrf2 expression which was confirmed by luciferase activity assay and western blot. What was more, consistent with miR140-5p expression, the mRNA and protein levels of Nrf2, as well as antioxidant response element (ARE)-driven genes Heme Oxygenase-1 (HO-1) and NAD(P)H:quinone oxidoreductase l (NQO1) were significantly increased in mice kidney tissues. In vitro study, Enforced expression of miR-140-5p in HK2 cells significantly attenuated oxidative stress by decreasing ROS level and increasing the expression of manganese superoxide dismutase (MnSOD). Simultaneously, miR-140-5p decreased lactate dehydrogenase (LDH) leakage and improved cell vitality in HK2 cells under Cisplatin-induced oxidative stress. However, HK2 cells transfected with a siRNA targeting Nrf2 abrogated the protective effects of miR-140-5p against oxidative stress. These results indicated that miR-140-5p might exert its anti-oxidative stress function via targeting Nrf2. Our findings showed the novel transcriptional role of miR140-5p in the expression of Nrf2 and miR-140-5p protected against Cisplatin induced oxidative stress by activating Nrf2-dependent antioxidant pathway, providing a potentially therapeutic target in acute kidney injury.
[Mh] Termos MeSH primário: Lesão Renal Aguda/induzido quimicamente
Elementos de Resposta Antioxidante/efeitos dos fármacos
Cisplatino/farmacologia
Citoproteção/genética
MicroRNAs/fisiologia
Fator 2 Relacionado a NF-E2/genética
Estresse Oxidativo/genética
[Mh] Termos MeSH secundário: Lesão Renal Aguda/genética
Lesão Renal Aguda/metabolismo
Animais
Elementos de Resposta Antioxidante/fisiologia
Células Cultivadas
Citoproteção/efeitos dos fármacos
Células HEK293
Seres Humanos
Proteína 1 Associada a ECH Semelhante a Kelch/fisiologia
Rim/efeitos dos fármacos
Rim/metabolismo
Rim/patologia
Masculino
Camundongos
Fator 2 Relacionado a NF-E2/metabolismo
Estresse Oxidativo/efeitos dos fármacos
Transdução de Sinais/efeitos dos fármacos
Transdução de Sinais/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Keap1 protein, mouse); 0 (Kelch-Like ECH-Associated Protein 1); 0 (MIRN140 microRNA, mouse); 0 (MicroRNAs); 0 (NF-E2-Related Factor 2); Q20Q21Q62J (Cisplatin)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171107
[Lr] Data última revisão:
171107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170921
[St] Status:MEDLINE


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[PMID]:28806787
[Au] Autor:Sheng XJ; Tu HJ; Chien WL; Kang KH; Lu DH; Liou HH; Lee MJ; Fu WM
[Ad] Endereço:Pharmacological Institute, College of Medicine, National Taiwan University, Taipei, Taiwan.
[Ti] Título:Antagonism of proteasome inhibitor-induced heme oxygenase-1 expression by PINK1 mutation.
[So] Source:PLoS One;12(8):e0183076, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:PTEN-induced putative kinase 1 (PINK1) is an integral protein in the mitochondrial membrane and maintains mitochondrial fidelity. Pathogenic mutations in PINK1 have been identified as a cause of early-onset autosomal recessive familial Parkinson's disease (PD). The ubiquitin proteasome pathway is associated with neurodegenerative diseases. In this study, we investigated whether mutations of PINK1 affects the cellular stress response following proteasome inhibition. Administration of MG132, a peptide aldehyde proteasome inhibitor, significantly increased the expression of heme oxygenase-1 (HO-1) in rat dopaminergic neurons in the substantia nigra and in the SH-SY5Y neuronal cell line. The induction of HO-1 expression by proteasome inhibition was reduced in PINK1 G309D mutant cells. MG132 increased the levels of HO-1 through the Akt, p38, and Nrf2 signaling pathways. Compared with the cells expressing WT-PINK1, the phosphorylation of Akt and p38 was lower in those cells expressing the PINK1 G309D mutant, which resulted in the inhibition of the nuclear translocation of Nrf2. Furthermore, MG132-induced neuronal death was enhanced by the PINK1 G309D mutation. In this study, we demonstrated that the G309D mutation impairs the neuroprotective function of PINK1 following proteasome inhibition, which may be related to the pathogenesis of PD.
[Mh] Termos MeSH primário: Regulação Enzimológica da Expressão Gênica/efeitos dos fármacos
Heme Oxigenase-1/metabolismo
Mutação/genética
Inibidores de Proteassoma/farmacologia
Proteínas Quinases/genética
Regulação para Cima/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Elementos de Resposta Antioxidante/genética
Morte Celular/efeitos dos fármacos
Linhagem Celular
Núcleo Celular/efeitos dos fármacos
Núcleo Celular/metabolismo
Seres Humanos
Leupeptinas/farmacologia
Masculino
Modelos Biológicos
Proteínas Mutantes/metabolismo
Fator 2 Relacionado a NF-E2/metabolismo
Neurônios/efeitos dos fármacos
Neurônios/metabolismo
Transporte Proteico/efeitos dos fármacos
Ratos Wistar
Transdução de Sinais/efeitos dos fármacos
Substância Negra/efeitos dos fármacos
Substância Negra/metabolismo
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Leupeptins); 0 (Mutant Proteins); 0 (NF-E2-Related Factor 2); 0 (Proteasome Inhibitors); EC 1.14.14.18 (Heme Oxygenase-1); EC 2.7.- (Protein Kinases); EC 2.7.11.1 (PTEN-induced putative kinase); RF1P63GW3K (benzyloxycarbonylleucyl-leucyl-leucine aldehyde)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171009
[Lr] Data última revisão:
171009
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170815
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0183076


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[PMID]:28684421
[Au] Autor:Perez-Leal O; Barrero CA; Merali S
[Ad] Endereço:From the Department of Pharmaceutical Sciences, Moulder Center for Drug Discovery Research, Temple University School of Pharmacy, Philadelphia, Pennsylvania 19140 operez@temple.edu.
[Ti] Título:Pharmacological stimulation of nuclear factor (erythroid-derived 2)-like 2 translation activates antioxidant responses.
[So] Source:J Biol Chem;292(34):14108-14121, 2017 Aug 25.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Nuclear factor (erythroid-derived 2)-like 2 (Nrf2) is the master regulator of the antioxidant response, and its function is tightly regulated at the transcriptional, translational, and post-translational levels. It is well-known that Nrf2 is regulated at the protein level by proteasomal degradation via Kelch-like ECH-associated protein 1 (Keap1), but how Nrf2 is regulated at the translational level is less clear. Here, we show that pharmacological stimulation increases Nrf2 levels by overcoming basal translational repression. We developed a novel reporter assay that enabled identification of natural compounds that induce Nrf2 translation by a mechanism independent of Keap1-mediated degradation. Apigenin, resveratrol, and piceatannol all induced Nrf2 translation. More importantly, the pharmacologically induced Nrf2 overcomes Keap1 regulation, translocates to the nucleus, and activates the antioxidant response. We conclude that translational regulation controls physiological levels of Nrf2, and this can be modulated by apigenin, resveratrol, and piceatannol. Also, targeting this mechanism with novel compounds could provide new insights into prevention and treatment of multiple diseases in which oxidative stress plays a significant role.
[Mh] Termos MeSH primário: Elementos de Resposta Antioxidante/efeitos dos fármacos
Antioxidantes/farmacologia
Núcleo Celular/efeitos dos fármacos
Regulação da Expressão Gênica/efeitos dos fármacos
Proteína 1 Associada a ECH Semelhante a Kelch/metabolismo
Fator 2 Relacionado a NF-E2/agonistas
[Mh] Termos MeSH secundário: Transporte Ativo do Núcleo Celular/efeitos dos fármacos
Apigenina/farmacologia
Sistemas CRISPR-Cas
Núcleo Celular/metabolismo
Genes Reporter/efeitos dos fármacos
Células HEK293
Células Hep G2
Seres Humanos
Proteína 1 Associada a ECH Semelhante a Kelch/antagonistas & inibidores
Proteína 1 Associada a ECH Semelhante a Kelch/genética
Luciferases/genética
Luciferases/metabolismo
Mutação
Fator 2 Relacionado a NF-E2/química
Fator 2 Relacionado a NF-E2/genética
Fator 2 Relacionado a NF-E2/metabolismo
Fragmentos de Peptídeos/química
Fragmentos de Peptídeos/genética
Fragmentos de Peptídeos/metabolismo
Complexo de Endopeptidases do Proteassoma/efeitos dos fármacos
Complexo de Endopeptidases do Proteassoma/metabolismo
Proteólise/efeitos dos fármacos
Proteínas Recombinantes de Fusão/química
Proteínas Recombinantes de Fusão/metabolismo
Bibliotecas de Moléculas Pequenas
Estilbenos/farmacologia
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antioxidants); 0 (KEAP1 protein, human); 0 (Kelch-Like ECH-Associated Protein 1); 0 (NF-E2-Related Factor 2); 0 (NFE2L2 protein, human); 0 (Peptide Fragments); 0 (Recombinant Fusion Proteins); 0 (Small Molecule Libraries); 0 (Stilbenes); 6KS3LS0D4F (3,3',4,5'-tetrahydroxystilbene); 7V515PI7F6 (Apigenin); EC 1.13.12.- (Luciferases); EC 3.4.25.1 (Proteasome Endopeptidase Complex); Q369O8926L (resveratrol)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170912
[Lr] Data última revisão:
170912
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170708
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M116.770925


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[PMID]:28655653
[Au] Autor:Tabei Y; Murotomi K; Umeno A; Horie M; Tsujino Y; Masutani B; Yoshida Y; Nakajima Y
[Ad] Endereço:Health Research Institute, National Institute of Advanced Industrial Science and Technology (AIST), 2217-14 Hayashi-cho, Takamatsu, Kagawa 761-0395, Japan.
[Ti] Título:Antioxidant properties of 5-hydroxy-4-phenyl-butenolide via activation of Nrf2/ARE signaling pathway.
[So] Source:Food Chem Toxicol;107(Pt A):129-137, 2017 Sep.
[Is] ISSN:1873-6351
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:5-Hydroxy-4-phenyl-butenolide (5H4PB) is a bioactive compound with antifungal and anti-obesity properties. Although it has recently been shown that 5H4PB activates peroxisome proliferator-activated receptor-gamma (PPARγ), the effect of 5H4PB on intracellular signaling pathways has not been clarified. In this study, we found that 5H4PB activated the nuclear factor erythroid 2-related factor 2 (Nrf2)/antioxidant response element (ARE) signaling pathway, which plays an important role in cellular defense against oxidative stress, and the subsequent upregulation of ARE-dependent cytoprotective genes, including the heme oxygenase-1, catalase, and superoxide dismutase genes, without exhibiting cytotoxicity. In addition, 5H4PB significantly attenuated intracellular ROS generation, glutathione oxidation, and DNA damage induced by hydrogen peroxide (H O ) exposure in mouse fibroblast cells. Furthermore, we demonstrated that pretreatment with 5H4PB confers a significant cytoprotective effect against H O -induced cell death in mouse cultured fibroblasts and primary hepatocytes. Thus, our study demonstrated that 5H4PB enhanced cellular resistance to oxidative damage via activation of the Nrf2/ARE signaling pathway.
[Mh] Termos MeSH primário: 4-Butirolactona/análogos & derivados
Elementos de Resposta Antioxidante/efeitos dos fármacos
Antioxidantes/farmacologia
Fator 2 Relacionado a NF-E2/metabolismo
[Mh] Termos MeSH secundário: 4-Butirolactona/farmacologia
Animais
Morte Celular/efeitos dos fármacos
Dano ao DNA/efeitos dos fármacos
Feminino
Heme Oxigenase-1/genética
Heme Oxigenase-1/metabolismo
Peróxido de Hidrogênio/metabolismo
Camundongos
Camundongos Endogâmicos ICR
Fator 2 Relacionado a NF-E2/genética
Estresse Oxidativo/efeitos dos fármacos
Espécies Reativas de Oxigênio/metabolismo
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (5-hydroxy-4-phenylbutenolide); 0 (Antioxidants); 0 (NF-E2-Related Factor 2); 0 (Nfe2l2 protein, mouse); 0 (Reactive Oxygen Species); BBX060AN9V (Hydrogen Peroxide); EC 1.14.14.18 (Heme Oxygenase-1); OL659KIY4X (4-Butyrolactone)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170829
[Lr] Data última revisão:
170829
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170629
[St] Status:MEDLINE


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[PMID]:28645578
[Au] Autor:Su C; Liu Z; Wang Y; Wang Y; Song E; Song Y
[Ad] Endereço:Key Laboratory of Luminescence and Real-Time Analytical Chemistry (Southwest University), Ministry of Education, College of Pharmaceutical Sciences, Southwest University, Chongqing, 400715, People's Republic of China; Institute for Drug and Instrument Control of Health Dept GLD of PLA, Beijing, 1000
[Ti] Título:The electrophilic character of quinones is essential for the suppression of Bach1.
[So] Source:Toxicology;387:17-26, 2017 Jul 15.
[Is] ISSN:1879-3185
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:The activation of nuclear factor erythroid 2-related factor 2 (Nrf2) is the most important cellular defense mechanisms against oxidative attack. BTB and CNC homology-1 (Bach1), like Kelch-like ECH-associated protein 1 (Keap1), is one of a negative regulator of Nrf2 that control antioxidant response elements (ARE)-dependent gene expressions. In the current study, we found that quinones show greater capacity than hydroquinones in nuclear Bach1 export, as well as ubiquitin-dependent Bach1 degradation in our experimental time frame. Consistently, quinones are easier than hydroquinones in Nrf2 activation and ARE-driven antioxidant protein expressions. Considering the redox cycling potential of quinone-hydroquinone couple, we investigated the effect of transit metal oxidation on the regulation of Nrf2 activity. As shown, Fe enhanced hydroquinone-induced Nrf2 activation and ARE-driven gene expressions, suggesting quinones rather than hydroquinone activate Nrf2 through Bach1 arylation. Taking together, our investigation illustrated that the electrophilic character of quinones ensure their conjugation with Bach1, which is important for the downregulation of Bach1 and the upregulation of Nrf2 signaling.
[Mh] Termos MeSH primário: Fatores de Transcrição de Zíper de Leucina Básica/metabolismo
Benzoquinonas/toxicidade
Proteínas de Grupos de Complementação da Anemia de Fanconi/metabolismo
Hepatócitos/efeitos dos fármacos
Hidroquinonas/toxicidade
Quinonas/toxicidade
[Mh] Termos MeSH secundário: Elementos de Resposta Antioxidante
Fatores de Transcrição de Zíper de Leucina Básica/genética
Regulação para Baixo
Proteínas de Grupos de Complementação da Anemia de Fanconi/genética
Glutationa/metabolismo
Células Hep G2
Hepatócitos/metabolismo
Seres Humanos
Ferro/metabolismo
Fator 2 Relacionado a NF-E2/metabolismo
Oxirredução
Ligação Proteica
Proteólise/efeitos dos fármacos
Transdução de Sinais/efeitos dos fármacos
Fatores de Tempo
Ubiquitinação/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (1,4-dihydroquinone); 0 (BACH1 protein, human); 0 (Basic-Leucine Zipper Transcription Factors); 0 (Benzoquinones); 0 (Fanconi Anemia Complementation Group Proteins); 0 (Hydroquinones); 0 (NF-E2-Related Factor 2); 0 (NFE2L2 protein, human); 0 (Quinones); C12674942B (2-tert-butylhydroquinone); E1UOL152H7 (Iron); F18QT8490S (2-tert-butyl-4-quinone); GAN16C9B8O (Glutathione)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170625
[St] Status:MEDLINE


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[PMID]:28599098
[Au] Autor:Zhao Y; Liu D; Proksch P; Yu S; Lin W
[Ad] Endereço:State Key Laboratory of Natural and Biomimetic Drugs, Peking University, Beijing, 100191, P. R. China.
[Ti] Título:Angupyrones A - E, α-Pyrone Analogues with ARE-Activation from a Sponge-Associated Fungus Truncatella angustata.
[So] Source:Chem Biodivers;14(9), 2017 Sep.
[Is] ISSN:1612-1880
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:TLC-DPPH guided fractionation of a sponge-associated fungus Truncatella angustata with a solid culture resulted in the isolation of five new α-pyrone-based analogues namely angupyrones A - E (1 - 5), and 3-ethyl-4-hydroxy-6-methyl-2-pyrone. Their structures were determined on the basis of extensive spectroscopic analyses, including the modified Mosher's method, bulkiness rule, and specific rotation for the configurational assignments. Angupyrones A - E exhibited moderate antioxidant response element activation in HepG2C8 cells, while the preliminary structure-activity relationship was discussed.
[Mh] Termos MeSH primário: Elementos de Resposta Antioxidante/efeitos dos fármacos
Antioxidantes/química
Antioxidantes/farmacologia
Poríferos/microbiologia
Pironas/química
Pironas/farmacologia
Xylariales/química
[Mh] Termos MeSH secundário: Animais
Antioxidantes/isolamento & purificação
Linhagem Celular
Seres Humanos
Pironas/isolamento & purificação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (4-hydroxy-6-methyl-2-pyrone); 0 (Antioxidants); 0 (Pyrones)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171006
[Lr] Data última revisão:
171006
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170610
[St] Status:MEDLINE
[do] DOI:10.1002/cbdv.201700236


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[PMID]:28583816
[Au] Autor:Xu W; Li F; Xu Z; Sun B; Cao J; Liu Y
[Ad] Endereço:Department of Neurosurgery, Qilu Hospital and Brain Science Research Institute of Shandong University, Jinan 250012, China. Electronic address: xuwenzhe2008@126.com.
[Ti] Título:Tert-butylhydroquinone protects PC12 cells against ferrous sulfate-induced oxidative and inflammatory injury via the Nrf2/ARE pathway.
[So] Source:Chem Biol Interact;273:28-36, 2017 Aug 01.
[Is] ISSN:1872-7786
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Increasing evidence had proved the critical role of iron in the pathogenesis of numerous neurodegenerative diseases because of its capacity to promote the formation of reactive oxygen species (ROS). Tert-butylhydroquinone (tBHQ) was a metabolite of butylated hydroxyanisole, a widely used food antioxidant. This study was aimed to investigate the protective effects of tBHQ on a cellular model of neurodegenerative disease, which was established in PC12 cells by exposure to ferrous sulfate (FS), and elucidate the potential protective mechanisms. The results showed that FS exposure increased lactate dehydrogenase (LDH) release and cell apoptosis in PC12 cells, accompanied by significant increases in the bax/bcl-2 ratio, cytochrome c release, and caspase-3 cleavage. It also enhanced the ROS production, malondialdehyde (MDA) content (lipid peroxidation), γ-H2A.X formation (DNA damage), and promoted nuclear factor kappa B (NF-κB) activation and expressions of cyclooxygenase-2 (COX-2), tumor necrosis factor-α (TNF-α) and interleukin-1ß (IL-1ß). tBHQ pretreatment alleviated FS-induced LDH release, cell apoptosis, oxidative stress and inflammatory response by promoting Nrf2 nuclear translocation and the protein levels of Nrf2 downstream target genes heme oxygenase-1 (Hmox-1), nicotinamide adenine dinucleotide phosphate (NADPH): quinone oxidoreductase-1 (Nqo1) and glutathione peroxidase-1 (Gpx1). tBHQ alleviated the FS-induced LDH release in control siRNA-treated PC12 cells, but failed to alleviate FS-induced LDH release in Nrf2 siRNA-treated cells. These findings suggested that pretreatment with tBHQ protected PC12 cells from FS-induced oxidative and inflammatory injury via the Nrf2/ARE pathway. tBHQ was promising as a potential therapeutic agent for neurodegenerative diseases induced by iron toxicity and should be encouraged for further research.
[Mh] Termos MeSH primário: Compostos Ferrosos/farmacologia
Hidroquinonas/farmacologia
Inflamação/tratamento farmacológico
Fator 2 Relacionado a NF-E2/metabolismo
Estresse Oxidativo/efeitos dos fármacos
Substâncias Protetoras/farmacologia
[Mh] Termos MeSH secundário: Animais
Elementos de Resposta Antioxidante/genética
Células PC12
Ratos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ferrous Compounds); 0 (Hydroquinones); 0 (NF-E2-Related Factor 2); 0 (Nfe2l2 protein, rat); 0 (Protective Agents); 39R4TAN1VT (ferrous sulfate); C12674942B (2-tert-butylhydroquinone)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171002
[Lr] Data última revisão:
171002
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170607
[St] Status:MEDLINE


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[PMID]:28550120
[Au] Autor:Staitieh BS; Ding L; Neveu WA; Spearman P; Guidot DM; Fan X
[Ad] Endereço:Division of Pulmonary, Allergy, Critical Care and Sleep Medicine, Emory University School of Medicine, Atlanta, Georgia, USA; bashar.staitieh@emory.edu.
[Ti] Título:HIV-1 decreases Nrf2/ARE activity and phagocytic function in alveolar macrophages.
[So] Source:J Leukoc Biol;102(2):517-525, 2017 Aug.
[Is] ISSN:1938-3673
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Respiratory complications occur frequently in individuals living with human immunodeficiency-1 virus (HIV) infection, and there is evidence that HIV-related oxidative stress impairs alveolar macrophage immune function. We hypothesized that nuclear factor (erythroid-derived 2)-like 2 (Nrf2), a master transcription factor that activates the antioxidant response element (ARE) and regulates antioxidant defenses, has an important role in alveolar macrophage (AMs) immune dysfunction in individuals with HIV infections. To test that hypothesis, we analyzed human monocyte-derived macrophages (MDMs) that were either infected with HIV-1 or were exposed to the HIV-related proteins gp120 and Tat ex vivo and determined that either stress affected the expression of Nrf2 and the Nrf2-ARE-dependent genes for NAD(P)H dehydrogenase, quinone 1 ( ) and glutamate-cysteine ligase, catalytic subunit ( ). We then determined that the expression of Nrf2, NQO1, and GCLC was significantly decreased in primary AMs isolated from HIV-1 transgenic rats. In parallel, treating a rat macrophage cell line (NR8383 cells) with the HIV-related proteins gp120 or Tat similarly decreased the gene and protein expression of Nrf2, NQO1, and GCLC. Further, phagocytic function was decreased in both human MDMs infected with HIV-1 and primary AMs from HIV-1 transgenic rats. Importantly, treating HIV-1-infected human MDMs or AMs from HIV-1 transgenic rats with sulforaphane (SFN, an Nrf2 activator) significantly improved their phagocytic function. The salutary effects of SFN were abrogated by silencing RNA to Nrf2 in wild-type rat macrophages. Our findings demonstrate that HIV-1 infection and exposure to HIV-1-related proteins inhibit Nrf2-ARE activity in the AMs and impair their phagocytic function. Treatments targeted at increasing Nrf2-ARE activity could, therefore, enhance lung innate immunity in people living with HIV-1.
[Mh] Termos MeSH primário: Elementos de Resposta Antioxidante/imunologia
Regulação da Expressão Gênica/imunologia
Infecções por HIV/imunologia
Macrófagos Alveolares/imunologia
Fator 2 Relacionado a NF-E2/imunologia
[Mh] Termos MeSH secundário: Animais
Western Blotting
HIV-1/imunologia
Seres Humanos
Macrófagos Alveolares/virologia
Fator 2 Relacionado a NF-E2/metabolismo
Fagocitose/imunologia
Ratos
Ratos Endogâmicos F344
Ratos Transgênicos
Reação em Cadeia da Polimerase em Tempo Real
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (NF-E2-Related Factor 2); 0 (NFE2L2 protein, human)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170925
[Lr] Data última revisão:
170925
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170528
[St] Status:MEDLINE
[do] DOI:10.1189/jlb.4A0616-282RR


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[PMID]:28493927
[Au] Autor:Kobatake E; Nakagawa H; Seki T; Miyazaki T
[Ad] Endereço:Milk Science Research Institute, Megmilk Snow Brand Co., Ltd., Saitama, Japan.
[Ti] Título:Protective effects and functional mechanisms of Lactobacillus gasseri SBT2055 against oxidative stress.
[So] Source:PLoS One;12(5):e0177106, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Lactobacillus gasseri SBT2055 (LG2055) is one of the probiotic lactic acid bacteria. Recently, we demonstrated that feeding with LG2055 extended the lifespan of Caenorhabditis elegans and that the prolongevity effect was dependent upon the regulation of oxidative stress response. In this study, we assessed whether LG2055 regulated the oxidative stress response of mammalian cells. In NIH-3T3 cells and primary mouse embryonic fibroblast cells, low cell proliferation rates and high reactive oxygen species levels were observed following paraquat treatment. LG2055 treatment suppressed these responses in paraquat-treated cells, indicating that LG2055 protected against oxidative stress in mammalian cells. The mRNA expression of oxidative stress-related genes, total nuclear factor-erythroid-2-related factor 2 (Nrf2) protein levels, and the nuclear translocation of Nrf2 were increased by LG2055 treatment. These results suggested that the Nrf2-antioxidant response element (ARE) signaling pathway was activated by LG2055. Furthermore, c-Jun NH2-terminal kinase (JNK) was activated by LG2055 treatment and the inhibition of JNK suppressed the activation of the Nrf2-ARE signaling pathway in LG2055-treated cells. Together, these findings suggest that LG2055 activated the Nrf2-ARE signaling pathway by JNK activation, thus strengthening the defense system against oxidative stress in mammalian cells.
[Mh] Termos MeSH primário: Fibroblastos/metabolismo
Fibroblastos/microbiologia
Lactobacillus gasseri/metabolismo
Estresse Oxidativo
Probióticos/metabolismo
[Mh] Termos MeSH secundário: Animais
Elementos de Resposta Antioxidante
Proliferação Celular
Células Cultivadas
Fibroblastos/citologia
Proteínas Quinases JNK Ativadas por Mitógeno/metabolismo
Sistema de Sinalização das MAP Quinases
Camundongos
Fator 2 Relacionado a NF-E2/genética
Fator 2 Relacionado a NF-E2/metabolismo
Células NIH 3T3
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (NF-E2-Related Factor 2); 0 (Nfe2l2 protein, mouse); EC 2.7.11.24 (JNK Mitogen-Activated Protein Kinases)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170919
[Lr] Data última revisão:
170919
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170512
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0177106



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