Butylphthalide alleviates sleep deprivation-induced cognitive deficit by regulating Nrf2/HO-1 pathway

Purpose: The purpose of this study was to assess the effects of butylphthalide on cognitive deficiencies following sleep deprivation (SD). Methods: The influence of butylphthalide on cognitive function changes in SD-induced mice was evaluated. Nissl staining and HE staining were used to analyze the morphology changes of the hippocampal formation. The changes in cognitive function of SD-induced mice were detected by the Morris water maze. Inflammatory factors, apoptosis, and signal pathway-related proteins in the mice hippocampus were detected. Results: SD increased escape latency and path length for mice to reach the hidden platform, decreased the time and range of activity in the target area, and reduced the number and time for traversing the target area. Butylphthalide significantly improved the cognitive decline of SD-induced spatial exploration and learning/memory ability. Butylphthalide also decreased the degeneration of hippocampal neurone, neuronal apoptosis, and inflammatory factors in hippocampus tissue. In addition, butylphthalide activated the nuclear factor erythroid 2-related factor (Nrf2)/heme oxygenase 1 (HO-1) pathway. Conclusion: Butylphthalide alleviated SD-induced cognitive decline, neuronal apoptosis, and inflammation by activating Nrf2/HO-1 pathway. We suggested that butylphthalide may be a prospective candidate for the alleviation of cognitive deficit induced by SD. (c) 2022 Elsevier B.V. All rights reserved.

Automated summary

This study assessed the effects of butylphthalide on cognitive deficiencies caused by sleep deprivation. The results showed that butylphthalide improved cognitive decline, reduced neuronal degeneration, apoptosis, and inflammation in the hippocampus. Activation of the Nrf2/HO-1 pathway was involved in the protective effects of butylphthalide.