Dexmedetomidine alleviates hippocampal damage in chronic sleep deprived rats by activating BDNF/TrkB signaling pathway
10.16557/j.cnki.1000-7547.2025.04.012
- VernacularTitle:右美托咪定激活BDNF/TrkB信号缓解慢性睡眠剥夺大鼠的海马损伤
- Author:
Biqiong ZHENG
1
;
Changyi LIU
;
Shuhui HU
Author Information
1. 福建医科大学附属第一医院麻醉科,福州 350005;福建医科大学附属第一医院滨海院区国家区域医疗中心麻醉科,福州 350212
- Publication Type:Journal Article
- Keywords:
chronic sleep deprivation(CSD);
dexmedetomidine(DEX);
BDNF/TrkB signal pathway;
caspase-3;
hippocampus;
rat
- From:
Chinese Journal of Neuroanatomy
2025;41(4):501-506
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To observe the protective effects and possible mechanisms of dexmedetomidine(DEX)on hippocampal tissues of chronic sleep deprived(CSD)rats.Methods:Healthy male rats were divided into Control group,CSD group,CSD+DEX group,DEX group,and CSD+DEX+ANA-12 group.The CSD model was established by the modified multi-platform method(MMPM),and the rats were deprived of sleep for 18 hours per day for 21 days.DEX was combined with tyrosine kinase receptor B antagonist(ANA-12)for intervention.Starting at 7 days post sleep deprivation for 14 days.At the end of modeling,brain-derived neurotrophic factor(BDNF)protein in hippocampal neu-rons was determined by immunohistochemical staining;pro-inflammatory cytokines in hippocampal tissue homogenates were assessed by enzyme-linked immunosorbent assay;tyrosine kinase receptor B(TrkB)signaling proteins and cyste-ine protein hydrolase 3(caspase-3)were detected by Western blot.Results:Compared with the Control group,the expression levels of IL-1β,IL-6,TNF-α and caspase-3 in the hippocampus of rats in the CSD group were significantly increased(P<0.05),while the expression level of BDNF in the hippocampal CA1 region was markedly reduced(P<0.05);Compared with the CSD group,the expression levels of IL-1β,IL-6,TNF-α and caspase-3 in the hippocampus of rats in the CSD+DEX group were significantly reduced(P<0.05),while the expression level of BDNF in the CA1 region of the hippocampus was markedly increased(P<0.05);Compared with the CSD+DEX group,the expression levels of IL-1β,IL-6,TNF-α and caspase-3 in the hippocampus of rats in the CSD+DEX+ANA-12 group were signifi-cantly increased(P<0.05),while the expression level of BDNF in the CA1 region of the hippocampus was markedly decreased(P<0.05).Conclusion:DEX inhibited CSD-induced hippocampal tissue damage.The possible mechanism is related to the regulation of BDNF/TrkB signaling by DEX.
