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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