Depression is caused by a variety of factors, especially stressful life events. Chronic stress-induced depression has detrimental effects on hippocampal integrity. Environmental enrichment (EE) is a beneficial intervention for improving anxiety, fear, and stress. We aimed to investigate the antidepressive effects of EE in a depressive rat model (DEP) that was subjected to chronic stress. The control group ( n = 10) was kept under normal conditions, while depressive rats ( n = 8 per group) were randomized into DEP, DEP + EE, and DEP + fluoxetine (Flx) groups. DEP + EE/Flx groups were exposed to standard housing and EE or Flx, respectively. The behavioral tests showed that hopelessness and anxiety were decreased in DEP + EE and DEP + Flx groups compared with the DEP group ( p < .05). Similarly, the expression of vascular endothelial growth factor and tryptophan hydroxylase was significantly higher in the DEP + EE and DEP + Flx ( p < .05) groups. The levels of brain-derived neurotrophic factor and tyrosine receptor kinase B were also significantly higher in the DEP + EE and DEP + Flx groups compared with the DEP group ( p < .05). Our findings can serve as a foundation for future investigations examining the effects of environmental improvement and physical exercise in patients with depression. This study suggests that EE may be useful for mitigating the detrimental effects of chronic stress in patients with depression.

Vascular dementia (VaD) is the second most common cause of dementia. It occurs when the cerebral blood supply is reduced by disarrangement of the circulatory system. Environmental enrichment (EE) has been associated with cognitive improvement, motor function recovery, and anxiety relief with respect to various neurodegenerative diseases and emotional stress models. The purpose of this study was to determine whether long-term EE influenced cognitive impairment in a rat model of chronic hypoperfusion induced by permanent occlusion of bilateral common carotid arteries (BCCAo). The Y-maze and Morris water maze tests were performed to evaluate the rats' cognitive functions. Also, the protein expression of brain-derived neurotrophic factor (BDNF), phosphorylated cAMP-calcium response element binding protein (pCREB), and vascular endothelial growth factor (VEGF) were confirmed by Western blot. The microvessels and angiogenesis-associated proteins in the hippocampal region were investigated using immunohistochemistry. The VaD + EE group showed significantly better cognitive functions than the VaD group in both the Y-maze and MWM tests. In addition, the VaD + EE group showed significantly increased expression of BDNF, pCREB, and VEGF in the hippocampus compared to the VaD group. Rats in the VaD + EE group also had increased length of microvessels and VEGF expression in the hippocampus. These results suggest that long-term EE exerts neuroprotective effects against cognitive impairment induced by chronic cerebral hypoperfusion through the enhancement of BDNF, pCREB, and VEGF expression and indicate that EE may be a good nursing intervention in vascular dementia patients.

Purpose: This study was done to identify whether pre-conditioning exercise has neuroprotective effects against cerebral ischemia, through enhance brain microvascular integrity. Methods: Adult male Sprague-Dawley rats were randomly divided into four groups: 1) Normal (n= 10); 2) Exercise (n= 10); 3) Middle cerebral artery occlusion (MCAo), n= 10); 4) Exercise+MCAo (n= 10). Both exercise groups ran on a treadmill at a speed of 15 m/min, 30 min/day for 4 weeks, then, MCAo was performed for 90 min. Brain infarction was measured by Nissl staining. Examination of the remaining neuronal cell after MCAo, and microvascular protein expression on the motor cortex, showed the expression of Neuronal Nuclei (NeuN), Vascular endothelial growth factor (VEGF) & laminin. Results: After 48 hr of MCAo, the infarct volume was significantly reduced in the Ex+MCAo group (15.6± 2.7%) compared to the MCAo group (44.9± 3.8%) (p< .05), and many neuronal cells were detected in the Ex+ MCAo group (70.8± 3.9%) compared to the MCAo group (43.4± 5.1%) (p< .05). The immunoreactivity of laminin, as a marker of microvessels and Vascular endothelial growth factor (VEGF) were intensively increased in the Ex+MCAo group compared to the MCAo group. Conclusion: These findings suggest that the neuroprotective effects of exercise pre-conditioning reduce ischemic brain injury through strengthening the microvascular integrity after cerebral ischemia.

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