An Overview of Stroke: Mechanism, In vivo Experimental Models Thereof, and Neuroprotective Agents

Curr Protein Pept Sci. 2020;21(9):860-877. doi: 10.2174/1389203721666200617133903.

Abstract

Background: Stroke is one of the causes of death and disability globally. Brain attack is because of the acute presentation of stroke, which highlights the requirement for decisive action to treat it.

Objective: The mechanism and in-vivo experimental models of stroke with various neuroprotective agents are highlighted in this review.

Method: The damaging mechanisms may proceed by rapid, nonspecific cell lysis (necrosis) or by the active form of cell death (apoptosis or necroptosis), depending upon the duration and severity and of the ischemic insult.

Results: Identification of injury mediators and pathways in a variety of experimental animal models of global cerebral ischemia has directed to explore the target-specific cytoprotective strategies, which are critical to clinical brain injury outcomes.

Conclusion: The injury mechanism, available encouraging medicaments thereof, and outcomes of natural and modern medicines for ischemia have been summarized. In spite of available therapeutic agents (thrombolytics, calcium channel blockers, NMDA receptor antagonists and antioxidants), there is a need for an ideal drug for strokes.

Keywords: Apoptosis; NMDA; bilateral common carotid artery occlusion; cerebral ischemia; necroptosis; neuroprotection; stroke.

Publication types

  • Review

MeSH terms

  • Animals
  • Antioxidants / pharmacology*
  • Apoptosis / drug effects
  • Apoptosis / genetics
  • Brain / drug effects
  • Brain / metabolism
  • Brain / pathology
  • Brain Ischemia / drug therapy*
  • Brain Ischemia / genetics
  • Brain Ischemia / metabolism
  • Brain Ischemia / pathology
  • Calcium Channel Blockers / pharmacology
  • Calcium Channels / genetics
  • Calcium Channels / metabolism
  • Disease Models, Animal
  • Fibrinolytic Agents / pharmacology
  • Gene Expression Regulation
  • Humans
  • Necroptosis / drug effects
  • Necroptosis / genetics
  • Necrosis / genetics
  • Necrosis / metabolism
  • Necrosis / pathology
  • Necrosis / prevention & control*
  • Neuroprotective Agents / pharmacology*
  • Nitric Oxide / metabolism
  • Receptors, N-Methyl-D-Aspartate / antagonists & inhibitors
  • Receptors, N-Methyl-D-Aspartate / genetics
  • Receptors, N-Methyl-D-Aspartate / metabolism
  • Signal Transduction
  • Stroke / drug therapy*
  • Stroke / genetics
  • Stroke / metabolism
  • Stroke / pathology

Substances

  • Antioxidants
  • Calcium Channel Blockers
  • Calcium Channels
  • Fibrinolytic Agents
  • Neuroprotective Agents
  • Receptors, N-Methyl-D-Aspartate
  • Nitric Oxide