Journal
INTERNATIONAL JOURNAL OF NEUROSCIENCE
Volume 131, Issue 7, Pages 641-649Publisher
TAYLOR & FRANCIS LTD
DOI: 10.1080/00207454.2020.1797722
Keywords
Post-stroke cognitive impairment (PSCI); middle cerebral artery occlusion (MCAO); enriched environment (EE); neuroinflammation; oxidative stress; astrocytes
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Funding
- Leading Personnel Training Project of Shanghai Pudong New District Municipal Health Bureau [PWR12018-04]
- Science and Technology Development Fund of Shanghai Pudong New District [PKJ2018-Y38]
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Enriched environment (EE) can improve cognitive function in post-stroke cognitive impairment (PSCI) rats by inhibiting neuroinflammation and oxidative stress.
Introduction Neuroinflammation and oxidative stress are major mechanisms of post-stroke cognitive impairment (PSCI) neural injury and decreased spatial and memory capacity. Enriched environment (EE) is an effective method to improve cognitive dysfunction. However, the regulation by EE of neuroinflammation, oxidative stress and associated mechanisms in animal models remains unclear. Materials and methods In this study, a rat PSCI model was established by middle cerebral artery occlusion (MCAO). Rats were randomly divided into the control group, standard environment (SE) group and EE group for 28 days. A Morris water-maze test was used to measure cognitive function at 7, 14 and 28 days after MCAO. Rats were sacrificed on the 28th day. Quantitative PCR, immunohistochemistry and ELISA were respectively used to detect mRNA expression of NF-E2-related factor 2 (Nrf2) and Nrf2 response genes, the expression of IL-1 beta and levels of proinflammatory cytokines in the hippocampus. Results EE improved mNSS scores and cognitive ability in PSCI rats. EE increased mRNA expression of the Nrf2 and Nrf2 response genes, including heme oxygenase-1 (HO-1) and NAD(P)H:quinone oxidoreductase 1 (NQO1). EE significantly decreased the level of malondialdehyde (MDA) and increased the levels of superoxide dismutase (SOD) and glutathione (GSH), in the hippocampus of PSCI rats. EE reduced the number of IL-1 beta positive cells in the hippocampus, and IL-1 beta levels in the hippocampus and serum. EE increased GFAP-positive astrocytes in the hippocampus, and BDNF levels in the hippocampus and serum. Conclusions EE can improve cognitive function in PSCI rats by inhibiting neuroinflammation and oxidative stress.
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