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ilg, brain, nrf, pubmed, nlrp, article, mgkg, injury, google, scholar, inflammasome, rats, cas, fig, sirna, nfκb, activation, effects, treatment, pathway, intracerebral, hemorrhage, levels, ros, cells, induction, early, results, significantly, isoliquiritigenin, protein, tissue, expression, staining, antioxidant, yang, administration, central, nuclear, min, antibody, oxidative, mechanisms, deficits, components, ilβ, cell, group, ratsgroup, experimental,

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quantitative real-time rt-pcr real-time rt-qpcr assay real-time rt-qpcr extracellular signal-regulated kinase1/2 nf-kappab-dependent autophagic pathway real-time quantitative pcr humidity-controlled specific pathogen-free goat anti-rabbit igg rabbit polyclonal anti-il-1β perform related rt-qpcr subsequent il-1β/il-18 release rabbit polyclonal anti-pycard rabbit polyclonal anti-myeloperoxidase rabbit polyclonal anti-nrf2 rabbit polyclonal anti-il-18 mouse monoclonal anti-cryopyrin mouse monoclonal anti-3-nitrotyrosine mouse monoclonal anti-8-hydroxyguanosine nf-kappab signal disruption enzyme-linked immunosorbent assay nrf2-mediated antioxidant system nrf2-induced antioxidant system lps-induced inflammatory responses ampk-mediated gsk3β inhibition ampk-mediated gsk3beta inhibition blood-brain barrier permeability s-allyl-l-cysteine autologous blood-imitated model nf-κb signaling pathways focal cerebral ischemia total nf-κb p65 blood-brain barrier disruption nrf2/antioxidant defense pathway nuclear nf-κb p65 article download pdf ros-induced brain injury central nervous system iron-catalyzed oxidative stress wet weight − dry weight nrf2 sirna + ilg 20 mg/kg collagenase-induced intracerebral hemorrhage wet/dry weight method dry/wet weight method key transcription factor ich-induced brain impairments nrf2-mediated counter-regulation central injury mechanism cytoplasmic nf-κb p65 pathway post lipopolysaccharide 40 mg/kg markedly alleviated

Schema {🗺️}

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         headline: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
         description:Intracerebral 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. ICH 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. ILG (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. Intraperitoneal 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.
         datePublished:2017-06-13T00:00:00Z
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            Early brain injury
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            NLRP3 inflammasome
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            Neurobiology
            Immunology
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      headline: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
      description:Intracerebral 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. ICH 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. ILG (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. Intraperitoneal 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.
      datePublished:2017-06-13T00:00:00Z
      dateModified:2017-06-13T00:00:00Z
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      pageEnd:19
      license:http://creativecommons.org/publicdomain/zero/1.0/
      sameAs:https://doi.org/10.1186/s12974-017-0895-5
      keywords:
         ICH
         Early brain injury
         ILG
         Nrf2
         ROS
         NF-κB
         NLRP3 inflammasome
         Neurosciences
         Neurology
         Neurobiology
         Immunology
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            name:Jun Zeng
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                  name:Southern Medical University
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      name:Department of Neurosurgery, Zhujiang Hospital, The National Key Clinical Specialty, The Neurosurgery Institute of Guangdong Province, Guangdong Provincial Key Laboratory on Brain Function Repair and Regeneration, The Engineering Technology Research Center of Education Ministry of China, Southern Medical University, Guangzhou, China
      name:Department of Neurosurgery, Zhujiang Hospital, The National Key Clinical Specialty, The Neurosurgery Institute of Guangdong Province, Guangdong Provincial Key Laboratory on Brain Function Repair and Regeneration, The Engineering Technology Research Center of Education Ministry of China, Southern Medical University, Guangzhou, China
      name:Department of Neurosurgery, Jingmen No. 1 People’s Hospital, Jingmen, China
      name:Department of Neurosurgery, Affiliated Hospital of Xiangnan University, Chenzhou, China
      name:Department of Neurosurgery, The Fifth Affiliated Hospital of Southern Medical University, Guangzhou, China
      name:Department of Neurosurgery, Gaoqing Campus of Central Hospital of Zibo, Gaoqing People’s Hospital, Zibo, China
      name:Department of Neurosurgery, 999 Brain Hospital, Jinan University, Guangzhou, China
      name:Department of Neurosurgery, Zhujiang Hospital, The National Key Clinical Specialty, The Neurosurgery Institute of Guangdong Province, Guangdong Provincial Key Laboratory on Brain Function Repair and Regeneration, The Engineering Technology Research Center of Education Ministry of China, Southern Medical University, Guangzhou, China
      name:Department of Neurosurgery, Zhujiang Hospital, The National Key Clinical Specialty, The Neurosurgery Institute of Guangdong Province, Guangdong Provincial Key Laboratory on Brain Function Repair and Regeneration, The Engineering Technology Research Center of Education Ministry of China, Southern Medical University, Guangzhou, China

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