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Environmental Enrichment Protects Against Cognition Deficits Caused by Sepsis-Associated Encephalopathy.
Tang, Yi-Fei; Duan, Ya-Jing; Ge, Rui-Dong; Lu, Xi; Gao, Bei-Yao; Guo, Jing-Wei; Jiang, Shan.
Afiliação
  • Tang YF; Department of Rehabilitation Medicine, The China-Japan Friendship Hospital, 100029 Beijing, China.
  • Duan YJ; Department of Rehabilitation Medicine, The China-Japan Friendship Hospital, 100029 Beijing, China.
  • Ge RD; Department of Rehabilitation Medicine, The China-Japan Friendship Hospital, 100029 Beijing, China.
  • Lu X; Department of Rehabilitation Medicine, The China-Japan Friendship Hospital, 100029 Beijing, China.
  • Gao BY; Department of Rehabilitation Medicine, The China-Japan Friendship Hospital, 100029 Beijing, China.
  • Guo JW; Department of Rehabilitation Medicine, The China-Japan Friendship Hospital, 100029 Beijing, China.
  • Jiang S; Department of Rehabilitation Medicine, The China-Japan Friendship Hospital, 100029 Beijing, China.
J Integr Neurosci ; 22(1): 5, 2022 Nov 29.
Article em En | MEDLINE | ID: mdl-36722228
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.
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Texto completo: 1 Base de dados: MEDLINE Assunto principal: Encefalopatias / Transtornos Cognitivos / Disfunção Cognitiva / Encefalopatia Associada a Sepse Tipo de estudo: Etiology_studies / Risk_factors_studies Limite: Animals Idioma: En Revista: J Integr Neurosci Assunto da revista: NEUROLOGIA Ano de publicação: 2022 Tipo de documento: Article País de afiliação: China

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Encefalopatias / Transtornos Cognitivos / Disfunção Cognitiva / Encefalopatia Associada a Sepse Tipo de estudo: Etiology_studies / Risk_factors_studies Limite: Animals Idioma: En Revista: J Integr Neurosci Assunto da revista: NEUROLOGIA Ano de publicação: 2022 Tipo de documento: Article País de afiliação: China