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Table 3 The relationship between inflammation and cognitive impairment in OSAS animal model

From: The relationship between inflammation and neurocognitive dysfunction in obstructive sleep apnea syndrome

Reference

Experiment animal

Control animal

Detecting parameter

Cognitive dysfunction

Results

Dong et al. 2018 [135]

V + CIH; SEV + CIH

V + RA; SEV + RA

TNF-α, IL-1β, activity of microglia, and expression and activity of PPAR-γ in hippocampus

Impaired spatial learning and memory in experiment group. SEV exaggerated the cognitive deficits

V + CIH showing increased TNF-α, IL-1β levels and microglia activity. SEV aggravated microglia-mediated inflammation via downregulation of PPAR-γ

Sapin et al. 2015 [136]

C57BL/6J mice + IH

C57BL/6J mice + RA

CCL5, MCP-1/CCL2, ICAM-1, TNF-α, IL-1β, IL-6 and IL-10 mRNA and microglial changes in the dH and vH regions of hippocampus

NA

Experiment group showing increased density and morphological features of microglia priming in dH; IL-1β and RANTES/CCL5 mRNA increased in dH of experiment group

Shi et al. 2018 [137]

C57BL/6J mice + IH; T2DM + IH

C57BL/6J mice + RA; T2DM + RA

Hippocampal neurons apoptosis, microglia activity, HMGB1, NF-κB-p65, TNF-α and IL-1β

Longer escape latency; Reduced numbers of platform crossing and percentage of time spent in the fourth quadrant in Morris water maze of experiment group

All the parameters were significantly increased in experiment group

Snyder et al. 2017 [138]

Adult male rats + CIH

Adult male rats + RA

IL-4, IL-5, IL-6, IL-10, IL-13, TNF-α and IFN-γ protein levels and OS levels in brain tissue

NA

Exposure to CIH increases inflammation and OS levels in brain regions associated with neurodegenerative diseases

Darnall et al. 2017 [139]

Rat pups + CIH

Rat pups + RA

Gro/CXCL1 in plasma; IFN-γ, IL-1β, IL-4, IL-5, IL-6, IL-10, IL-13, KC/GRO and TNF-α in brain tissue and NSE

NA

Increased plasma levels of Gro/CXCL1, cerebellar levels of IFN-γ and IL-1β and NSE in rat pups + CIH

Kim et al. 2013 [140]

ALS + CIH; Wt-CIH

ALS + RA; Wt-RA

NF-κB inhibitor alpha, 4-HNE, anti-GFAP and motor neuron counts

Impaired spatial memory in mice exposed to CIH

ALS + CIH showing poor motor learning and spatial memory, higher levels of OS and inflammation and elevated motor neuron death

Block et al. 2003 [141]

Adult rats + IH

Adult rats + RA

Gene expression of TLR4 and mRNA levels of iNOS, COX-2, TNF-α, IL-1β and IL-6 in microglia

NA

All the parameters showing increase in IH group

Deng et al. 2015 [142]

V + CIH; atorvastatin + CIH

V + RA; atorvastatin + RA

TNF-α, IL-1β, MDA, SOD; expression of TLR4, MyD88 and TRIF mRNA and protein; neuronal cell damage in hippocampus CA1 region

NA

All parameters except SOD were increased in V + CIH mice. V + CIH showing lower SOD level. Atorvastatin attenuated all these changes

Burckhardt et al. 2008 [143]

V + IH; GTP + IH

V + RA; GTP + RA

PGE2, RAGE, the ratio of RAGE/β-actin, GFAP, MDA, and p47phox in brain tissue

GTP attenuated IH-induced spatial learning deficits

All parameters were significantly increased in brain tissue of experiment group. GTP alleviated the IH induced inflammation and OS in the brain

Lam et al. 2015 [144]

V + CIH; LBPs + CIH

V + RA; LBPs + RA

TNF-α, IL-1β, COX-2, NFκB, MDA, antioxidant enzymes (SOD, GPx-1), ER stress and apoptosis in the hippocampus

LBPs reversed CIH-induced spatial memory deficits

V + CIH showing increased levels of TNF-α, IL-1β, COX-2, NFκB, ER stress, OS and neuronal apoptosis in hippocampus. LBPs decreased inflammation and OS levels and improved cognitive deficits

Deng et al. 2015 [145]

V + CIH; BBG + CIH

V + RA; BBG + RA

P2X7R mRNA and protein, NFκB, TNF-α, IL-β, IL-6, IL-18, NOX2, SOD, MDA in the hippocampus

BBG improved spatial learning performance in mice exposed to CIH

All parameters showing highest increases in the hippocampus of V + CIH; BBG alleviated CIH induced inflammation, OS, neural injury and cognition deficits

Yuan et al. 2015 [146]

V + CIH; Telmisartan + CIH

V + RA; Telmisartan + RA

Plasma CRP and IL-6; MDA, NOS, NO and apoptosis in hippocampal CA1 region

NA

All parameters showing highest increases in V + CIH. Telmisartan decreased inflammation and OS levels and hippocampal apoptosis

Row et al. 2004 [147]

PAFR–/– mice + IH; Wt + IH

PAFR–/– mice +RA; Wt +RA

NOS activity, COX-2 and PGE2 in cortical; caspase 3 in cortex and CA1 region of hippocampus

Impaired spatial learning showing in Wt + IH but not PAFR–/– mice + IH

Wt + IH showing the highest levels of all the parameters. PAFR–/– alleviated neuroinflammation and apoptosis in the brain

  1. V + CIH vehicle + CIH, Wt-CIH wild-type + CIH, PAFR–/–mice + IH platelet-activating factor receptor deficient mice + IH, NA not administrated, CIH chronic intermittent hypoxia, RA room air, SEV sevoflurane, ALS amyotrophic lateral sclerosis, GTP green tea catechin polyphenols, LBPs Lycium barbarum polysaccharides, BBG Brilliant Blue G, TNF-α tumor necrosis factor-α, IL interleukin, PPAR-γ peroxisome proliferators-activated receptor γ, CCL5 CC motif chemokine ligand 5, MCP-1/CCL2 monocyte chemoattractant protein-1/CC motif chemokine ligand 2, ICAM-1 intercellular adhesion molecules-1, HMGB1 high mobility group box 1, NF-κB nuclear factor kappa B, IFN-γ interferon-γ, OS oxidative stress, GFAP glial fibrillary acidic protein, NSE neuron-specific enolase, 4-HNE 4-hydroxynonenal, TLR4 toll-like receptor-4, iNOS inducible nitric oxide synthase, NOS nitric oxide synthase, COX-2 cyclooxygenase-2, MDA malondialdehyde, SOD superoxide dismutase, GPx-1 glutathione peroxidase-1, MyD88 myeloid differentiation factor 88, TRIF TIR domain-containing adaptor inducing interferon-β, NOX2 NADPH oxidase 2, PGE2 prostaglandin E2, RAGE receptor for advanced glycation end product, ER stress endoplasmic reticulum stress, P2X7R P2X7 receptor