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Omentin-1 May Be One Treatment Factor for Intravenous Thrombolysis of Acute Cerebral Infarction Through the Inhibition of NLRP3 Ubiquitination by AMPK Function: Preliminary Findings.

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  • المؤلفون: Xu J;Xu J; Huang S; Huang S
  • المصدر:
    Neurology India [Neurol India] 2024 Mar 01; Vol. 72 (2), pp. 309-318. Date of Electronic Publication: 2024 Apr 30.
  • نوع النشر :
    Journal Article
  • اللغة:
    English
  • معلومة اضافية
    • المصدر:
      Publisher: Medknow Publications Country of Publication: India NLM ID: 0042005 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1998-4022 (Electronic) Linking ISSN: 00283886 NLM ISO Abbreviation: Neurol India Subsets: MEDLINE
    • بيانات النشر:
      Publication: Mumbai : Medknow Publications
      Original Publication: Bombay : Neurological Society of India
    • الموضوع:
    • نبذة مختصرة :
      Background: Acute cerebral infarction (ACI) is a common neurological disease that is associated with high morbidity, disability and mortality rates. At present, antiplatelet therapy is a necessary treatment for ACI. The present study aimed to investigate the effects of omentin-1 on the intravenous thrombolysis of ACI.
      Objective: The present study aimed to investigate the effects of omentin-1 on the intravenous thrombolysis of ACI.
      Material and Methods: The mouse model of ACI was induced using male C57BL/6 mice through middle cerebral artery occlusion (MCAO). Meanwhile, the murine BV2 microglial cells were pretreated with 0.1 mg/ml of lipopolysaccharide (LPS), and then induced with 2 mM of adenosine triphosphate (ATP).
      Results: The omentin-1 mRNA expression in patients receiving intravenous thrombolysis for ACI was down-regulated compared with the normal group. Additionally, the serum level of omentin-1 was negatively correlated with National Institute of Health Stroke Scale (NIHSS) score or serum level of IL-1β or MMP-2 in patients receiving intravenous thrombolysis for ACI. Meanwhile, the serum mRNA expression of omentin-1 was positively correlated with Barthel index or high-sensitivity C-reactive protein (hs-CRP) in patients undergoing intravenous thrombolysis for ACI. As observed from the in vitro model, Omentin-1 reduced inflammation, promoted cell growth, alleviated ROS-induced oxidative stress, and enhanced AMPK activity through activating NLRP3 ubiquitination. Omentin-1 presented ACI in the mouse model of ACI. Regulating AMPK activity contributed to controlling the effects of Omentin-1 on the in vitro model.
      Conclusions: Omentin-1 reduced neuroinflammation and ROS-induced oxidative stress in the mouse model of ACI, which was achieved by inhibiting NLRP3 ubiquitination through regulating AMPK activity. Therefore, omentin-1 may serve as a treatment factor for the intravenous thrombolysis of ACI in further clinical application.
      (Copyright © 2024 Copyright: © 2024 Neurology India, Neurological Society of India.)
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    • الرقم المعرف:
      0 (Cytokines)
      0 (NLR Family, Pyrin Domain-Containing 3 Protein)
      0 (GPI-Linked Proteins)
      0 (Lectins)
      0 (ITLN1 protein, human)
      EC 2.7.11.31 (AMP-Activated Protein Kinases)
      0 (Itln1 protein, mouse)
      0 (Nlrp3 protein, mouse)
    • الموضوع:
      Date Created: 20240501 Date Completed: 20240501 Latest Revision: 20240702
    • الموضوع:
      20240702
    • الرقم المعرف:
      10.4103/ni.ni_1325_21
    • الرقم المعرف:
      38691475