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已发表论文
右美托咪定通过激活脑源性神经营养因子/酪氨酸激酶受体 B 信号通路减轻快速眼动睡眠剥夺大鼠海马组织损伤
Received 28 May 2025
Accepted for publication 16 September 2025
Published 1 October 2025 Volume 2025:17 Pages 2423—2435
DOI https://doi.org/10.2147/NSS.S539185
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 3
Editor who approved publication: Dr Sarah L Appleton
Biqiong Zheng,1,2,* Yang Li,3,* Changyi Liu4,5
1Department of Anesthesiology, The First Affiliated Hospital of Fujian Medical University, Fuzhou, 350005, People’s Republic of China; 2Department of Anesthesiology, National Regional Medical Center, Binhai Campus of The First Affiliated Hospital, Fujian Medical University, Fuzhou, 350212, People’s Republic of China; 3Department of Anesthesiology, The First Affiliated Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, Fujian Province, 361001, People’s Republic of China; 4Department of Urology, The First Affiliated Hospital of Fujian Medical University, Fuzhou, 350005, People’s Republic of China; 5Department of Urology, National Regional Medical Center, Binhai Campus of The First Affiliated Hospital, Fujian Medical University, Fuzhou, 350212, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Changyi Liu, Department of Urology, The First Affiliated Hospital of Fujian Medical University, Fuzhou, No. 20, Cha Zhong Road, Fuzhou, Fujian Province, People’s Republic of China, Email lcy900125@fjmu.edu.cn
Introduction: Sleep deprivation often leads to marked neurobehavioral and cognitive deficits, yet few well-defined interventions exist to address these effects. Dexmedetomidine (DEX), a highly selective α2-adrenoceptor agonist, possesses sedative, hypnotic, analgesic, and sympathetic-blocking properties, closely mimic natural sleep state. In this study, we aim to investigate whether DEX protects hippocampal tissue against rapid eye movement sleep deprivation (RSD)-induced injury in rats and to explore the underlying molecular mechanisms.
Methods: In this study, a rapid eye movement sleep deprivation (RSD) rat model was created using a modified multi-platform method. The influence of dexmedetomidine (DEX) on hippocampal tissue morphology, the BDNF/TrkB signaling pathway, and cognitive function was then evaluated. Group comparisons were analyzed using one-way ANOVA followed by appropriate post hoc tests.
Results: In comparison with the control group, DEX significantly alleviated the impaired spatial learning and memory as reflected escape latency and increased the time spent in the garget quadrant. ANA-12 reversed these improvements, indicating DEX’s cognitive benefits. HE staining showed that DEX protected neurons from RSD-induced injury by preserving structural integrity and TUNEL assay demonstrated reduced neuron apoptosis in the DEX group. Co-treatment with ANA-12 abolished these protective effects, resulting in neuronal damage and apoptosis levels similar to those observed in RSD rats. Moreover, compared with the level of TNA alpha in RSD rats, IL 6, IL 1beta and MDA levels were lower in the hippocampus of DEX group, while SOD activity was enhanced. Western blot analysis revealed that DEX increased hippocampal BDNF (0.586 ± 0.036 vs 0.315 ± 0.034, ~1.86 fold, P < 0.01), TrkB (0.774 ± 0.039 vs 0.518 ± 0.033, ~1.49 fold, P < 0.01) and pro-TrkB expression. However, co-administration of ANA 12 abolished these effects, returning expression levels close to those in the RSD group, implying that DEX’s neuroprotection is mediated via the BDNF/TrkB pathway.
Conclusion: These findings indicate that DEX exerts neuroprotective effects in RSD by activating the BDNF/TrkB pathway, offering valuable evidence for DEX-based therapeutic approaches to sleep deprivation-related brain injury.
Keywords: dexmedetomidine, rapid eye movement sleep deprivation, hippocampus, BDNF, TrkB, neuroprotection
1Department of Anesthesiology, The First Affiliated Hospital of Fujian Medical University, Fuzhou, 350005, People’s Republic of China; 2Department of Anesthesiology, National Regional Medical Center, Binhai Campus of The First Affiliated Hospital, Fujian Medical University, Fuzhou, 350212, People’s Republic of China; 3Department of Anesthesiology, The First Affiliated Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, Fujian Province, 361001, People’s Republic of China; 4Department of Urology, The First Affiliated Hospital of Fujian Medical University, Fuzhou, 350005, People’s Republic of China; 5Department of Urology, National Regional Medical Center, Binhai Campus of The First Affiliated Hospital, Fujian Medical University, Fuzhou, 350212, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Changyi Liu, Department of Urology, The First Affiliated Hospital of Fujian Medical University, Fuzhou, No. 20, Cha Zhong Road, Fuzhou, Fujian Province, People’s Republic of China, Email lcy900125@fjmu.edu.cn
Introduction: Sleep deprivation often leads to marked neurobehavioral and cognitive deficits, yet few well-defined interventions exist to address these effects. Dexmedetomidine (DEX), a highly selective α2-adrenoceptor agonist, possesses sedative, hypnotic, analgesic, and sympathetic-blocking properties, closely mimic natural sleep state. In this study, we aim to investigate whether DEX protects hippocampal tissue against rapid eye movement sleep deprivation (RSD)-induced injury in rats and to explore the underlying molecular mechanisms.
Methods: In this study, a rapid eye movement sleep deprivation (RSD) rat model was created using a modified multi-platform method. The influence of dexmedetomidine (DEX) on hippocampal tissue morphology, the BDNF/TrkB signaling pathway, and cognitive function was then evaluated. Group comparisons were analyzed using one-way ANOVA followed by appropriate post hoc tests.
Results: In comparison with the control group, DEX significantly alleviated the impaired spatial learning and memory as reflected escape latency and increased the time spent in the garget quadrant. ANA-12 reversed these improvements, indicating DEX’s cognitive benefits. HE staining showed that DEX protected neurons from RSD-induced injury by preserving structural integrity and TUNEL assay demonstrated reduced neuron apoptosis in the DEX group. Co-treatment with ANA-12 abolished these protective effects, resulting in neuronal damage and apoptosis levels similar to those observed in RSD rats. Moreover, compared with the level of TNA alpha in RSD rats, IL 6, IL 1beta and MDA levels were lower in the hippocampus of DEX group, while SOD activity was enhanced. Western blot analysis revealed that DEX increased hippocampal BDNF (0.586 ± 0.036 vs 0.315 ± 0.034, ~1.86 fold, P < 0.01), TrkB (0.774 ± 0.039 vs 0.518 ± 0.033, ~1.49 fold, P < 0.01) and pro-TrkB expression. However, co-administration of ANA 12 abolished these effects, returning expression levels close to those in the RSD group, implying that DEX’s neuroprotection is mediated via the BDNF/TrkB pathway.
Conclusion: These findings indicate that DEX exerts neuroprotective effects in RSD by activating the BDNF/TrkB pathway, offering valuable evidence for DEX-based therapeutic approaches to sleep deprivation-related brain injury.
Keywords: dexmedetomidine, rapid eye movement sleep deprivation, hippocampus, BDNF, TrkB, neuroprotection