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Expression Changes of Neuroprotective Signaling Molecules in the Mouse Cortex Following Permanent Middle Cerebral Artery Occlusion - Neuroprotective Signaling In pMCAO -

  • Anatomy & Biological Anthropology
  • Abbr : Anat Biol Anthropol
  • 2026, 39(3), pp.251~258
  • DOI : 10.11637/aba.2026.39.3.251
  • Publisher : 대한체질인류학회
  • Research Area : Medicine and Pharmacy > Anatomy
  • Received : July 24, 2026
  • Accepted : August 18, 2026
  • Published : June 30, 2026

Hwang Hyo In ORD ID 1,  Park Junghee 1,  신혜경 ORD ID 1,  Yoon-Young Chung ORD ID 1,  KIM DONGJOON 1,  JUN, YONGHYUN ORD ID 1

1조선대학교 의과대학

Accredited

ABSTRACT

Oxidative stress and altered intracellular signaling contribute to ischemic brain injury; however, molecular alterations during the subacute phase following permanent cerebral ischemia remain incompletely understood. In this study, nine-week-old male mice underwent permanent middle cerebral artery occlusion using the intraluminal filament method, and ipsilateral cortical tissue was collected three days after ischemia. Western blot analysis was performed to evaluate nuclear factor erythroid 2-related factor 2, heme oxygenase-1, brain- derived neurotrophic factor, and the activation of protein kinase B and extracellular signal-regulated kinase. Nuclear factor erythroid 2-related factor 2 and heme oxygenase-1 expression levels were significantly decreased following permanent cerebral ischemia, whereas brain-derived neurotrophic factor expression was significantly increased. Protein kinase B activation, assessed by the ratio of its phosphorylated to total form, was significantly reduced, whereas extracellular signal-regulated kinase activation showed no significant difference between the control and ischemia groups. These findings demonstrate distinct alterations in antioxidant defense, neurotrophic responses, and intracellular survival signaling in the cerebral cortex three days after permanent cerebral ischemia and provide insight into molecular responses associated with the subacute stage of ischemic injury.

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