Effects of an enriched environment on cognition and sonic hedgehog signaling after cerebral ischemia
10.3760/cma.j.issn.0254-1424.2024.05.001
- VernacularTitle:丰富环境康复训练对脑缺血大鼠认知功能及音猬因子信号通路的影响
- Author:
Aiyan YU
1
;
Ziyu CHANG
;
Naiju ZHANG
;
Shoufeng CHEN
;
Xiaodong SONG
;
Lei XU
Author Information
1. 蚌埠医学院第一附属医院康复医学科，蚌埠 233004
- Keywords:
Stroke;
Cognitive dysfunction;
Brain ischemia;
Enriched environments
- From:
Chinese Journal of Physical Medicine and Rehabilitation
2024;46(5):385-392
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To observe any effect of an enriched environment (EET) on cognitive functioning and sonic hedgehog (SHH) signaling in rats modeling cerebral ischemia.Methods:Sixty adult male Sprague-Dawley rats were randomly divided into a blank control group, a model group and a training group. A model of cerebral ischemia was established in the model and training groups by thread thrombus. The training group was given an EET. After 7 and 14 days, the rats′ cognition was tested using the Morris water maze and the platform jumping test. Apoptosis of brain cells in the hippocampus was detected by using TUNEL staining, and the expression of SHH, Gli2 and PTCH1 proteins in the hippocampus were measured using qRT-PCRs, western blotting and immunohistochemistry.Results:After 14 days the average escape latency in the Morris water maze test had shortened more in the training group than in the model group, while the average swimming speed, the number of platform crossings and the time spent in the quadrant had increased significantly more. They also received fewer electric shocks and spent significantly less time on the platform in the platform jumping test on average. Apoptosis in the hippocampus after 14 days was significantly less in the training group with significantly greater expression of SHH and Gli2 protein and significantly less PTCH1 protein expression.Conclusion:An EET can significantly improve cognition after cerebral ischemia, at least in rats. Its mechanism may be related to enhanced activation of the SHH signaling pathway.
