Sigma-1 receptor alleviates postoperative cognitive dysfunction exacerbated by preoperative acute sleep deprivation in mice via modulating the Keap1/Nrf2 signaling pathway

Postoperative cognitive dysfunction (POCD) is a common neurological complication severely affecting patient prognosis. Preoperative acute sleep deprivation, a frequent perioperative stressor, significantly exacerbates POCD severity. Sigma-1 receptor (σ-1R), an endoplasmic reticulum molecular chaperone, plays a crucial role in modulating neuroinflammation and oxidative stress. However, whether σ-1R can serve as an interventional target to mitigate sleep deprivation-aggravated cognitive impairment remains insufficiently elucidated. This study aimed to clarify the regulatory role of σ-1R in a mouse model combining preoperative sleep deprivation with exploratory laparotomy, focusing on Keap1/Nrf2 signaling, and to evaluate its clinical translational potential. Behavioral, molecular biological, and morphological methods were utilized. Sleep deprivation exacerbated postoperative cognitive impairment, accompanied by a compensatory upregulation of σ-1R expression in hippocampal microglia. Notably, exogenous potentiation of σ-1R with the agonist PRE-084 reversed cognitive deficits, suppressed neuroinflammation and oxidative stress, promoted Nrf2 nuclear translocation, and upregulated downstream genes HO-1 and NQO1; conversely, the antagonist BD-1047 worsened the damage. Mechanistically, σ-1R physically associated with Keap1, promoting Nrf2 release. The Nrf2 inhibitor ML385 blocked PRE-084's protective effects. In vitro experiments confirmed PRE-084 alleviated inflammation and oxidative stress via an Nrf2-dependent pathway. Moreover, σ-1R signaling may partially contribute to the neuroprotective effects of dexmedetomidine. In conclusion, this study reveals that σ-1R activation is associated with protective effects in sleep deprivation-exacerbated POCD, potentially through regulating the Keap1/Nrf2 signaling pathway, a mechanism rarely reported in this context, suggesting σ-1R as a potential avenue for further investigation in POCD prevention.

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Journal
Neurotherapeutics
Published
2026-10-29
DOI
https://doi.org/10.1016/j.neurot.2026.e01109
Primary Topic
Pharmacological Receptor Mechanisms and Effects
Type
article
Field-Weighted Citation Impact
0.00

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article

Sigma-1 receptor alleviates postoperative cognitive dysfunction exacerbated by preoperative acute sleep deprivation in mice via modulating the Keap1/Nrf2 signaling pathway

Yalan Li, Xiuhua Li, Liang Xu, JiaTai An et al.
5 links
Neurotherapeutics
Pharmacological Receptor Mechanisms and Effects
article

Sigma-1 receptor alleviates postoperative cognitive dysfunction exacerbated by preoperative acute sleep deprivation in mice via modulating the Keap1/Nrf2 signaling pathway

Yalan Li, Xiuhua Li, Liang Xu, JiaTai An, Baorui Guo, Yuansong Wei, Jin Yu, Peng Li, Aiping Zheng
article en

Abstract

Postoperative cognitive dysfunction (POCD) is a common neurological complication severely affecting patient prognosis. Preoperative acute sleep deprivation, a frequent perioperative stressor, significantly exacerbates POCD severity. Sigma-1 receptor (σ-1R), an endoplasmic reticulum molecular chaperone, plays a crucial role in modulating neuroinflammation and oxidative stress. However, whether σ-1R can serve as an interventional target to mitigate sleep deprivation-aggravated cognitive impairment remains insufficiently elucidated. This study aimed to clarify the regulatory role of σ-1R in a mouse model combining preoperative sleep deprivation with exploratory laparotomy, focusing on Keap1/Nrf2 signaling, and to evaluate its clinical translational potential. Behavioral, molecular biological, and morphological methods were utilized. Sleep deprivation exacerbated postoperative cognitive impairment, accompanied by a compensatory upregulation of σ-1R expression in hippocampal microglia. Notably, exogenous potentiation of σ-1R with the agonist PRE-084 reversed cognitive deficits, suppressed neuroinflammation and oxidative stress, promoted Nrf2 nuclear translocation, and upregulated downstream genes HO-1 and NQO1; conversely, the antagonist BD-1047 worsened the damage. Mechanistically, σ-1R physically associated with Keap1, promoting Nrf2 release. The Nrf2 inhibitor ML385 blocked PRE-084's protective effects. In vitro experiments confirmed PRE-084 alleviated inflammation and oxidative stress via an Nrf2-dependent pathway. Moreover, σ-1R signaling may partially contribute to the neuroprotective effects of dexmedetomidine. In conclusion, this study reveals that σ-1R activation is associated with protective effects in sleep deprivation-exacerbated POCD, potentially through regulating the Keap1/Nrf2 signaling pathway, a mechanism rarely reported in this context, suggesting σ-1R as a potential avenue for further investigation in POCD prevention.

NeurotherapeuticsVol. 24(1)
Academy of Military Medical Sciences (CN), Chinese PLA General Hospital (CN), First Affiliated Hospital of Jinan University (CN)
Natural Science Foundation of Beijing Municipality, Natural Science Foundation of Shaanxi Province, Guangzhou Municipal Science and Technology Project
Good health and well-being
Openalex Percentile: Top 23%
Pharmacological Receptor Mechanisms and Effects
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