Protective Effect and Mechanism of Anmeidan against Neuronal Damage in Rat Model of Sleep Deprivation Based on Hippocampal Neuroinflammation
10.13422/j.cnki.syfjx.20250137
- VernacularTitle:基于海马神经炎症探讨安寐丹对睡眠剥夺大鼠模型神经元损伤的保护作用及机制
- Author:
Guangjing XIE
1
;
Zixuan XU
1
;
Junlu ZHANG
1
;
Jian ZHANG
2
;
Jing XIA
1
;
Bo XU
1
Author Information
1. Hubei University of Chinese Medicine， Wuhan 430065， China
2. Hubei Provincial Hospital of Traditional Chinese Medicine， Wuhan 430074， China
- Publication Type:Journal Article
- Keywords:
Anmeidan;
sleep deprivation;
neuroinflammation;
neuroprotection;
NOD-like receptor protein 3 （NLRP3） signaling pathway
- From:
Chinese Journal of Experimental Traditional Medical Formulae
2025;31(10):65-71
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo investigate the effects of Anmeidan （AMD） on neuroinflammation in the hippocampus of sleep-deprived rats. MethodsSD rats were randomly divided into four groups （n = 10 per group）： control group， model group， AMD group， and melatonin group. A sleep deprivation model was established using the modified multiple platform water environment method. The AMD group received AMD at a dose of 18.18 g·kg-1·d-1， the melatonin group received melatonin at 100 mg·kg-1·d-1， and the control and model groups were given an equal volume of pure water. All treatments were administered by gavage for four weeks. Spontaneous activity was assessed using an animal behavior video system. Serum levels of interleukin-1β （IL-1β）， interleukin-6 （IL-6）， and tumor necrosis factor-α （TNF-α） were measured by enzyme-linked immunosorbent assay （ELISA）. Hippocampal pyramidal neuron morphology was examined using hematoxylin-eosin （HE） staining， and ultrastructural changes of hippocampal neurons were observed via transmission electron microscopy. Immunofluorescence was used to detect the expression of brain-derived neurotrophic factor （BDNF） and nerve growth factor （NGF） in the hippocampus. Western blot analysis was performed to measure the expression of nuclear factor-κB （NF-κB）， phosphorylated NF-κB （p-NF-κB）， NOD-like receptor protein 3 （NLRP3）， and Caspase-1 proteins. ResultsCompared with the control group， the model group showed a significant increase in activity duration and frequency （P<0.01）， increased hippocampal pyramidal cell structural damage and decreased cell count， aggravated hippocampal ultrastructural damage， mitochondrial cristae disruption， and exacerbated vacuolization. The expression of p-NF-κB p65， NLRP3， and Caspase-1 proteins was upregulated， serum IL-1β， IL-6， and TNF-α levels were significantly elevated （P<0.01）， and the fluorescence intensity of BDNF and NGF proteins was significantly reduced （P<0.01）. Compared with the model group， the AMD group showed a significant reduction in activity duration and frequency （P<0.01）， increased hippocampal pyramidal cell count with reduced structural damage， alleviated hippocampal ultrastructural damage， significantly downregulated p-NF-κB p65， NLRP3， and Caspase-1 protein expression （P<0.01）， decreased serum IL-1β， IL-6， and TNF-α levels （P<0.01）， and significantly increased the fluorescence intensity of BDNF and NGF proteins （P<0.01）. ConclusionAnmeidan alleviates hippocampal neuronal damage in sleep-deprived rats， potentially by downregulating the NLRP3 signaling pathway， reducing inflammatory cytokine release， and increasing neurotrophic factor levels.
