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Published on: June 23, 2015
The effect of stress on stroke recovery in a photothrombotic stroke animal model
Zhen Jin1, Jinzi Wu, Sun-Young Oh
1Department of Medical Science, Chonbuk National University Graduate School, Jeonju, Chonbuk, Republic of Korea.
Insights
Restraint stress worsened stroke outcomes in rats, increasing infarct volume and delaying functional recovery. Stress modulated mitogen-activated protein kinase (MAPK) pathways, impacting stroke severity.
Area of Science:
- Neuroscience
- Cardiovascular Research
- Stress Physiology
Background:
- Psychosocial factors, chronic stress, and emotional states are established predictors of atherosclerosis and cardiovascular events.
- Despite their significance, psychosocial factors are often overlooked in clinical medical settings.
- This study investigates the impact of stress on ischemic brain injury.
Purpose of the Study:
- To evaluate the influence of acute stress on photothrombotic ischemic cortical injury in a rat model.
- To determine how stress affects behavioral function, infarct volume, and cellular apoptosis post-stroke.
- To examine the modulation of mitogen-activated protein kinase (MAPK) pathways by stress in stroke.
Main Methods:
- Sprague-Dawley rats were subjected to photothrombotic cortical injury and assigned to four groups.
- Restraint stress was applied for five days to specific stress groups.
- Evaluations included behavioral function, infarct volume, apoptotic cell death, and MAPK (Erk1/Erk2, p38MAPK) activation.
Main Results:
- Restraint stress significantly increased cortical infarct volume and apoptotic cell death in stroke models (p<0.05, p<0.01).
- Functional recovery was significantly impaired in the stress group compared to controls (p<0.05).
- Stress altered MAPK pathway activation, decreasing Erk1/Erk2 in stroke-stress groups and p38MAPK activation in stroke-stress groups compared to stroke controls.
Conclusions:
- Restraint stress exacerbates ischemic cortical injury and impairs functional recovery in a rat stroke model.
- Stress modulates the MAPK signaling pathway, contributing to altered stroke outcomes.
- These findings highlight the critical role of stress in stroke pathophysiology and recovery.
Background And Aims:
Several studies have provided convincing evidence that psychosocial factors, chronic stress and emotional factors are all independent predictors of atherosclerosis and cardiovascular events as well. However, psychosocial factors have received little attention in the medical setting. The purpose of this study is to evaluate the influence of stress on photothrombotic ischemic cortical injury in an animal model.
Methods:
Sprague-Dawley rats were assigned to the four groups and cortical photothrombosis was induced in the sensorimotor cortex. The stress groups were subjected to restraint stress for five days. We evaluate the behavioral function, infarct volume, apoptotic cell death and the activations of mitogen-activated protein kinases (MAPK: Erk1/Erk2, and p38MAPK) for the evaluation of stress effects on stroke.
Results:
There was a significant increase in cortical infarct volume and apoptotic cell death at the stroke group subjected to restraint stress (p<0.05, and p<0.01, respectively). The functional recovery was worst in restraint stress group during five days (p<0.05). The activation of Erk1 and Erk2 were increased by restraint stress in sham operation group but decreased in stroke-stress group than stroke control group (p<0.01). The activation of p38MAPK was increased by stroke but this effect was decreased by restraint stress (p<0.05, and p<0.01, respectively). Our data demonstrates that restraint stress increases infarction volume and decreases functional recovery in rat stroke models by modulation of the MAPK pathway.
