Poststroke cognitive impairment is a common complication in ischemic stroke patients, and its prevalence ranges from 25% to 30% (Kalaria et al., 2016). This study was approved by the Animal Ethics Committee of Fudan University of China (approval No. The efficacy of environmental enrichment combined with fasudil treatment was superior to that of fasudil treatment alone. These findings suggest that environmental enrichment combined with fasudil treatment can ameliorate memory dysfunction through inhibition of the hippocampal ROCK/cofilin pathway, alteration of the dynamic distribution of F-actin, and inhibition of neuronal death in the hippocampal CA1 region. Furthermore, the performance of mouse stroke models in the tail suspension test and step-through passive avoidance test improved significantly. After exposure to environmental enrichment combined with fasudil treatment, the number of neurons in the hippocampal CA1 region increased significantly, the expression and proportion of p-cofilin in the hippocampus decreased, and the distribution of F-actin in the hippocampal CA1 region increased significantly. Twenty-four hours after modeling, these animals were intraperitoneally administered fasudil (10 mg/kg) once daily for 14 successive days and/or provided with environmental enrichment for 21 successive days. A photothrombotic stroke model was established in 6-week-old male C57BL/6 mice. However, the efficacy of environmental enrichment combined with fasudil treatment remains poorly understood. An enriched environment can reduce poststroke cognitive impairment. Fasudil downregulates ROCK activation and protects neurons against cytoskeleton collapse in the acute phase after stroke. Dysfunction of the actin cytoskeleton correlates well with poststroke cognitive declines, and its reorganization requires proper regulation of Rho-associated kinase (ROCK) proteins. Currently, no specific treatment exists to promote recovery from cognitive impairment after a stroke.
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