Evidence map›Paper›PMID 42553001›Full record

ArticleBrain and behavior2026

Intermittent Hypoxia Exacerbates Lipopolysaccharide-Induced Neurobehavioral Abnormalities: The Role of Neuroinflammation and Synaptic-Related Proteins.

Yi-Zhu Ding, Zong-Fang Wang, Chen Dai, Yuan-Zi Ye

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Article in Brain and behavior, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

4 authors.

Yi-Zhu DingDepartment of Infectious Diseases, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui, People's Republic of China.
Zong-Fang WangDepartment of Neurological Surgery, Anhui No. 2 Provincial People's Hospital, Hefei, Anhui, People's Republic of China.
Chen DaiThoracic Surgery Department, Anhui Chest Hospital, Hefei, Anhui, People's Republic of, China.
Yuan-Zi YeDepartment of Pathology, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui, People's Republic of China.

Funding

Young Investigator Cultivation Fund of the First Affiliated Hospital of Anhui Medical University 2020kj01Young Investigator Cultivation Fund of the First Affiliated Hospital of Anhui Medical University (2020kj01)
6 · The paper itself

Abstract

backgroundSepsis is a common systemic inflammatory disease clinically observed in patients with severe trauma or infectious diseases. Lipopolysaccharide (LPS) serves as a classic tool for studying infection-related neuroinflammation and behavioral changes. Research indicates that LPS can induce peripheral inflammation and neuroinflammation, leading to synaptic dysfunction and neurobehavioral abnormalities. Furthermore, studies suggest that stress can increase susceptibility to inflammation. Intermittent hypoxia, a core pathological feature of obstructive sleep apnea syndrome, induces low-grade chronic inflammation in the central nervous system.

objectiveThis study investigates whether intermittent hypoxia exacerbates LPS-induced cognitive impairment, depression, and anxiety-like behaviors, and explores its potential mechanisms.

methodsAdult mice were treated with LPS alone or in combination with daily 8-h intermittent hypoxia via a hypoxia chamber. Depression and anxiety-like behavior were assessed using the tail suspension, forced swim, elevated plus maze, and open field tests. Spatial learning and memory were measured using the Morris water maze test. Pro-inflammatory cytokines and levels of genes and proteins of synaptic-related proteins were detected using enzyme-linked immunosorbent assay, western blotting, and real-time fluorescence-based quantitative PCR, respectively.

resultsLPS-induced impaired cognitive function, increased depression-like and anxiety-like behaviors, elevated pro-inflammatory cytokines, and decreased mRNA and protein levels of synapse-related proteins, synaptosomal-associated protein of 25 kDa, synaptotagmin-1, synaptophysin, and postsynaptic density protein-95 in adult male mice. Intermittent hypoxia exacerbated these adverse effects.

conclusionIntermittent hypoxia exacerbates LPS-induced neurobehavioral abnormalities, which are associated with neuroinflammation and alterations in synapse-related proteins.

Indexed as

Behavior, AnimalCognitive DysfunctionHypoxiaNeuroinflammatory DiseasesAnimalsAnxietyCytokinesDepressionDisease Models, AnimalInflammationLipopolysaccharidesMaleMaze LearningMiceMice, Inbred C57BLSynapsesCytokinesLipopolysaccharidescognitionintermittent hypoxialipopolysaccharideneuroinflammationsynaptic proteins

Identifiers

PMID42553001
PMCPMC13439392

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.