Rho-Kinase inhibition decreases focal cerebral ischemia-induced glial activation in rats.

Background: Rho-kinase inhibition in a rat middle cerebral artery occlusion (MCAO) model is reported to improve neurological functions and decrease infarction size. Objective: The objective of this study is to investigate the underlying mechanisms of such improvement by evaluating the effects of Rho...

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Publicado en:Journal of Central Nervous System Disease pp. 1 - 12
Autores principales: Sheikh, Abdullah Md, Yano, Shozo, Mitaki, Shingo, Tabassum, Shatera, Yamaguchi, Shuhei, Nagai, Atsushi
Formato: diagnostic images pictorial research tables/charts Journal Article
Publicado: Sage Publications Inc. 9/8/2022
Acceso en línea:Ver este registro en EBSCOhost
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      dt: 9/8/2022
      pid: 344
      pub: Sage Publications Inc.
      place: Thousand Oaks, California
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        10.1177/11795735221123910
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        atl: Rho-Kinase inhibition decreases focal cerebral ischemia-induced glial activation in rats.
      aug:
        au:
          Sheikh, Abdullah Md
          Yano, Shozo
          Mitaki, Shingo
          Tabassum, Shatera
          Yamaguchi, Shuhei
          Nagai, Atsushi
        affil: Department of Laboratory Medicine, 175764 Shimane University Faculty of Medicine, Izumo, Japan
      sug:
        subj:
          Cerebral Ischemia Complications
          Glial Cells Pathology
          Phosphotransferases
          Animal Studies
          Rats
          Blotting, Western
          Magnetic Resonance Imaging
          Cell Migration Assays
          In Vitro Studies
          RNA, Messenger Analysis
          Analysis of Variance
          T-Tests
          Descriptive Statistics
          P-Value
          Data Analysis Software
      ab: Background: Rho-kinase inhibition in a rat middle cerebral artery occlusion (MCAO) model is reported to improve neurological functions and decrease infarction size. Objective: The objective of this study is to investigate the underlying mechanisms of such improvement by evaluating the effects of Rho-kinase inhibition on astrocytes and microglial accumulation and activation in this condition. Methods: Adult male Sprague-Dawley (SD) rats were used to generate the MCAO model, which received an I.P injection of a chemical Rho-kinase inhibitor (Fasudil- 5 mg/kg/day) or vehicle (PBS) for 2 and 4 days. Results: Fasudil treatment significantly decreased the stroke volumes and water content in the lesion areas, as revealed by MRI. Immunostaining and Western blotting results demonstrated that Fasudil significantly decreased the levels of Aquaporin-4, a water channel protein. The number of GFAP+ astrocytes and Iba-1+ macrophage/microglia was decreased in the lesion areas. Proinflammatory transcription factor NF-κB protein levels were decreased in the Fasudil group 2 days after MCAO. Also, proinflammatory mediators including TNF-α, IL-1β, and iNOS levels were decreased. In vitro migration study using a human microglial cell line (HMO6) confirmed the inhibitory effects of Fasudil on the process. Fasudil also decreased combined IL-1β and IFNγ-induced NF-κB nuclear translocation in HMO6. Moreover, Fasudil transiently decreased combined IL-1β and IFNγ-induced iNOS, TNFα, and IL-1β mRNA levels in HMO6. Conclusion: Our study demonstrates the inhibitory effects of Rho-kinase on NF-κB-mediated glial activation and cerebral edema, which might be a promising therapeutic target in acute cerebral ischemia conditions.
      pubtype: Academic Journal
      doctype:
        diagnostic images
        pictorial
        research
        tables/charts
        Journal Article
      ougenre: Article
    language: English
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