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Related Concept Videos

Ischemic Stroke ll: Pathophysiology01:15

Ischemic Stroke ll: Pathophysiology

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An ischemic stroke occurs when a cerebral blood vessel becomes obstructed, most often by a thrombus or embolus, interrupting the delivery of oxygen and glucose to brain tissue. Because neurons rely on continuous aerobic metabolism, energy failure begins within minutes of reduced perfusion. The region receiving the least blood flow becomes the infarct core, an area of irreversible cellular death. Surrounding this core lies the penumbra, a zone of hypoperfused but still viable tissue that is...
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Early Ischemia and Ionic ImbalanceWithin minutes of spinal cord injury, a secondary cascade begins, progressing over hours to weeks. Vascular damage reduces blood flow, causing ischemia and mitochondrial dysfunction. ATP depletion leads to ion pump failure, membrane depolarization, sodium influx, potassium efflux, and water accumulation, resulting in cellular swelling. Increased intracellular calcium further disrupts mitochondria and accelerates cellular injury.Excitotoxicity and Neuronal...
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Hemorrhagic Stroke ll: Pathophysiology01:29

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A hemorrhagic stroke develops when a cerebral blood vessel ruptures, allowing blood to escape into the surrounding brain tissue, as in intracerebral hemorrhage (ICH), or into the subarachnoid space, as in subarachnoid hemorrhage (SAH). Because the skull is a rigid compartment, the sudden presence of extravascular blood rapidly increases intracranial pressure and compresses adjacent neural structures, leading to immediate tissue injury and impaired cerebral perfusion.Mass Effect and Primary...
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The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
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Ischemic Stroke l: Introduction01:15

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Ischemic stroke is an acute cerebrovascular condition in which blood flow to a brain region is suddenly interrupted, leading to tissue infarction. Neurons depend on continuous oxygen and glucose supply, so even brief reductions in perfusion cause energy failure, ionic imbalance, and irreversible injury. Ischemic strokes are classified into thrombotic and embolic types based on their underlying mechanisms.Thrombotic MechanismsThrombotic stroke develops when a clot forms within a cerebral artery.
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Targeting PTGS2/NF-κB Pathway: MG-132's Role in Reducing Ischemic Stroke Injury.

Yong-Sheng Wang1,2, Yuan-Cheng Huang3, Yong-Qi Wang4

  • 1Zhongshan Hospital (Xiamen), Fudan University, Xiamen, 361015, China.

Biochemical Genetics
|June 7, 2025
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The proteasome inhibitor MG-132 shows neuroprotective effects against ischemic stroke by reducing inflammation and oxidative stress. This finding offers a new therapeutic strategy for stroke recovery.

Keywords:
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Area of Science:

  • Neuroscience
  • Pharmacology
  • Biochemistry

Background:

  • Ischemic stroke is a major global health concern with limited treatment options.
  • Neuroinflammation and oxidative stress are key pathological processes in ischemic stroke-reperfusion (I/R) injury.
  • Developing effective neuroprotective agents targeting these pathways is critical.

Purpose of the Study:

  • To identify therapeutic targets for ischemic stroke using bioinformatics analysis.
  • To investigate the neuroprotective potential of MG-132, a proteasome inhibitor, in an ischemic stroke model.
  • To elucidate the underlying mechanisms of MG-132's neuroprotective effects.

Main Methods:

  • Bioinformatics analysis to identify differentially expressed genes (DEGs) and hub genes in ischemic stroke.
  • Utilized middle cerebral artery occlusion/reperfusion (MCAO/R) models in rodents.
  • Assessed infarct size, cerebral edema, neurological function, inflammatory markers, oxidative stress, and apoptosis.

Main Results:

  • MG-132 treatment significantly reduced infarct volume, cerebral edema, and improved neurological outcomes in MCAO/R models.
  • MG-132 downregulated PTGS2 expression and inhibited NF-κB activation, decreasing pro-inflammatory cytokines (TNF-α, IL-1β, IL-17).
  • MG-132 alleviated oxidative stress (reduced MDA) and apoptosis (decreased TUNEL-positive cells).

Conclusions:

  • MG-132 demonstrates significant neuroprotection in ischemic stroke by modulating the PTGS2/NF-κB pathway.
  • MG-132 effectively targets neuroinflammation and oxidative stress, key contributors to I/R injury.
  • These findings support MG-132 as a potential therapeutic agent for ischemic stroke.