title: Inflammation induced by increased frequency of intermittent hypoxia is attenuated by tempol administration.
abstract: The levels of serum inflammatory cytokines and the activation of nuclear factor kappa B (NF-κB) and hypoxia inducible factor-1α (HIF-1α) in heart tissues in response to different frequencies of intermittent hypoxia (IH) and the antioxidant tempol were evaluated. Wistar rats (64 males, 200-220 g) were randomly divided into 6 experimental groups and 2 control groups. Four groups were exposed to IH 10, 20, 30, or 40 times/h. The other 2 experimental groups were challenged with IH (30 times/h) plus tempol, either beginning on day 0 (IH30T0) or on day 29 (IH30T29). After 6 weeks of challenge, serum levels of tumor necrosis factor (TNF)-α, intracellular adhesion molecule (ICAM)-1, and interleukin-10 were measured, and western blot analysis was used to detect NF-κB p65 and HIF-1α in myocardial tissues. Serum levels of TNF-α and ICAM-1 and myocardial expression of NF-κB p65 and HIF-1α were all significantly higher in IH rats than in controls (P<0.001). Increased IH frequency resulted in more significant changes. Administration of tempol in IH rats significantly reduced levels of TNF-α, ICAM-1, NF-κB and HIF-1α compared with the non-tempol-treated group (F=16.936, P<0.001). IH induced an inflammatory response in a frequency-dependent manner. Additionally, HIF-1α and NF-κB were increased following IH administration. Importantly, tempol treatment attenuated this effect.
authors.affiliation: Department of Respiratory, Tianjin Medical University General Hospital, Tianjin, China.
authors.forename: J
authors.initials: J
authors.lastname: Zhang
authors.affiliation: Department of Respiratory, Tianjin Medical University General Hospital, Tianjin, China.
authors.forename: L
authors.initials: L
authors.lastname: Zheng
authors.affiliation: Department of Respiratory, Tianjin Medical University General Hospital, Tianjin, China.
authors.forename: J
authors.initials: J
authors.lastname: Cao
authors.affiliation: Department of Respiratory, Tianjin Medical University General Hospital, Tianjin, China.
authors.forename: B
authors.initials: B
authors.lastname: Chen
authors.affiliation: Department of Respiratory, Tianjin Medical University General Hospital, Tianjin, China.
authors.forename: D
authors.initials: D
authors.lastname: Jin
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000008:administration & dosage*; D001784:Blood Gas Analysis; D015153:Blotting, Western; D003497:Cyclic N-Oxides / Q000008:administration & dosage*; D004797:Enzyme-Linked Immunosorbent Assay; D000860:Hypoxia / Q000097:blood / Q000150:complications*; D051795:Hypoxia-Inducible Factor 1, alpha Subunit / Q000032:analysis; D007249:Inflammation / Q000378:metabolism / Q000517:prevention & control*; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood; D016753:Interleukin-10 / Q000097:blood; D008297:Male; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D016328:NF-kappa B / Q000032:analysis; D017208:Rats, Wistar; D013113:Spin Labels; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D000975:Antioxidants; D003497:Cyclic N-Oxides; D051795:Hypoxia-Inducible Factor 1, alpha Subunit; D016328:NF-kappa B; D013113:Spin Labels; D014409:Tumor Necrosis Factor-alpha; D018799:Intercellular Adhesion Molecule-1; D016753:Interleukin-10; C001803:tempol