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Related Concept Videos

Ischemic Stroke ll: Pathophysiology01:15

Ischemic Stroke ll: Pathophysiology

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...
Ischemic Stroke l: Introduction01:15

Ischemic Stroke l: Introduction

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.
Liver Regeneration01:24

Liver Regeneration

The liver is an important organ in vertebrates that plays an essential role in metabolism. It is also responsible for storing and redistributing nutrients such as carbohydrates, fats, and vitamins in the body. Additionally, the liver releases bile salts which are critical for digesting food and eliminating toxic metabolites from the body.
Cells of Liver
The liver comprises four major types of cells— hepatocytes, stellate, Kupffer, and sinusoidal endothelial cells. The hepatocytes are large...

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Related Experiment Video

Updated: Jul 1, 2026

Induction of Acute Ischemic Stroke in Mice Using the Distal Middle Artery Occlusion Technique
07:34

Induction of Acute Ischemic Stroke in Mice Using the Distal Middle Artery Occlusion Technique

Published on: December 15, 2023

Activation of liver X receptors promotes neuroprotection and reduces brain inflammation in experimental stroke.

Jesús R Morales1, Iván Ballesteros, José Manuel Deniz

  • 1Department of Pharmacology, School of Medicine, Universidad Complutense de Madrid, 28040 Madrid, Spain.

Circulation
|September 17, 2008
PubMed
Summary
This summary is machine-generated.

Liver X receptors (LXRs) agonists protect against stroke by reducing brain inflammation and infarct size. This study shows LXR signaling is crucial for neuroprotection after ischemic injury.

More Related Videos

A Preclinical Model to Assess Brain Recovery After Acute Stroke in Rats
10:15

A Preclinical Model to Assess Brain Recovery After Acute Stroke in Rats

Published on: November 6, 2019

Related Experiment Videos

Last Updated: Jul 1, 2026

Induction of Acute Ischemic Stroke in Mice Using the Distal Middle Artery Occlusion Technique
07:34

Induction of Acute Ischemic Stroke in Mice Using the Distal Middle Artery Occlusion Technique

Published on: December 15, 2023

A Preclinical Model to Assess Brain Recovery After Acute Stroke in Rats
10:15

A Preclinical Model to Assess Brain Recovery After Acute Stroke in Rats

Published on: November 6, 2019

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Immunology

Background:

  • Liver X receptors (LXRs) are nuclear receptors regulating cholesterol metabolism and inflammation.
  • LXRs exhibit anti-inflammatory properties in immune cells.
  • The role of LXRs in acute brain injury like stroke remains unclear.

Purpose of the Study:

  • To investigate LXR expression and function in experimental stroke.
  • To evaluate the therapeutic potential of LXR agonists in stroke models.

Main Methods:

  • Studied LXR expression and function in rat and mouse models of middle cerebral artery occlusion.
  • Administered synthetic LXR agonists (GW3965, TO901317) post-ischemia.
  • Utilized LXRalpha,beta(-/-) knockout mice for loss-of-function studies.

Main Results:

  • LXR agonist treatment significantly reduced infarct volume and improved neurological scores in rats.
  • Neuroprotection correlated with decreased brain proinflammatory gene expression and NF-kappaB activity.
  • LXRalpha,beta(-/-) mice showed exacerbated infarct size and inflammation, confirming endogenous LXR pathway involvement.

Conclusions:

  • LXR signaling acts as a protective pathway against brain injury.
  • LXR agonists demonstrate therapeutic potential for treating stroke.