Environmental Enrichment Protects Against Cognition Deficits Caused by Sepsis-Associated Encephalopathy

Abstract

Background: One of the most serious complications of sepsis is sepsis-associated encephalopathy (SAE), which impairs the cognition ability of survivors. Environmental enrichment (EE) has been demonstrated to alleviate cognition deficits under many kinds of brain injury conditions. However, EE's effects on SAE remain unknown. Therefore, this study aimed to determine EE's effect on cognition disorders under SAE conditions and the underlying mechanism. Materials and Methods: Adult male rats, subject to SAE or not, were housed under a standard environment (SE) or EE for 30 days. Subsequently, the rats were subjected to cognitive tests, such as the novel object recognition (NOR) test, the Morris water maze (MWM) test, an Open Field (OF) test, the elevated plus maze (EPM) test, and a sensory neglect (SN) test. Neuroinflammation, apoptosis, and oxidative stress changes in the brain were also detected. Results: The results revealed that SAE impaired somatesthesia, recognition memory, spatial learning and memory, and exploratory activity, which were significantly improved by EE housing. EE also prevented SAE-induced anxiety-like behavior. In addition, EE housing capable induced a decrease in pro-inflammatory cytokines, and an increase in anti-inflammatory cytokines and antioxidant properties in the brain. Moreover, EE housing exerted an anti-apoptosis function by upregulating the level of B-cell lymphoma/leukemia-2 (Bcl-2) level and downregulating the level of p53 level in the hippocampus. Conclusions: The results of the present study indicated that EE exerts a neuroprotective function on cognitive ability in SAE rats. The effect is achieved by increasing antioxidants, and anti-inflammatory and antiapoptotic capacities. EE can effectively rescue SAE-induced cognitive deficits.

An enriched environment ameliorates maternal sleep deprivation-induced cognitive impairment in aged mice by improving mitochondrial function via the Sirt1/PGC-1α pathway

“…Consistent with this observation, we found that SD during late pregnancy resulted in oxidative stress and neuroinflammation in the hippocampus and prefrontal cortex in aged offspring, as evidenced by the increased levels of ROS and MDA, decreased SOD activity, and upregulation of the levels of Iba-1 and IL-1β, IL-6, and TNF-α. EE could improve cognitive impairment by inhibiting neuroinflammation and oxidative stress [ 39 ]. For example, an enriched environment was reported to improve middle cerebral artery occlusion-induced cognition impairment in Sprague–Dawley rats by suppressing neuroinflammation and oxidative stress and increasing the expression levels of synaptic plasticity-related proteins in the hippocampus [ 25 ].…”