The effect of stress on stroke recovery in a photothrombotic stroke animal model

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.

Research Highlights
► We evaluate the effect of restraint stress on stroke recovery.
► Restraint stress increased the infarct volume and apoptotic cell death.
► Stressed-rat showed unfavorable outcome in beam-walking, beam-balance, and corner test.
► Spontaneous recovery of gross motor function was faster than that of coordination.
► Restraint stress decreased the activation of Erk1/Erk2 and p38MAPK in infarct core.