title: Single-dose oral quercetin improves redox status but does not affect heat shock response in mice.
abstract: Inflammation and oxidative stress are considered as likely contributors to heat injury. However, their roles in regulating the heat shock response in vivo remain unclear. We tested the hypothesis that acute quercetin treatment would improve redox status and reduce heat shock responses in mice. Mice underwent two heat tests before and after single oral administration of either quercetin (15 mg/kg) or vehicle. We measured physiologic and biochemical responses in mice during and 18 to 22 hours after heat tests, respectively. There were no significant differences in core temperature, heart rate, or blood pressure between quercetin and vehicle groups during heat exposure. Mice with relatively severe hyperthermia during the pretreatment heat test showed a significant trend toward a lower peak core temperature during the heat test after quercetin treatment. Compared with mice not exposed to heat, quercetin-treated mice had significantly lower interleukin 6 (P < .01) and higher superoxide dismutase levels (P < .01), whereas vehicle-treated mice had significantly lower total glutathione and higher 8-isoprostane levels in the circulation after heat exposure. Heat exposure significantly elevated heat shock proteins (HSPs) 72 and 90 and heat shock factor 1 levels in mouse liver, heart, and skeletal muscles, but no significant differences in tissue HSPs and heat shock factor 1 were found between quercetin- and vehicle-treated mice. These results suggest that a single moderate dose of quercetin is sufficient to alter redox status but not heat stress response in mice. Acute adaptations of peripheral tissues to heat stress may not be mediated by systemic inflammatory and redox state in vivo.
authors.affiliation: Department of Military and Emergency Medicine, Uniformed Services University of the Health Sciences, Bethesda, MD, USA. Electronic address: yifan.chen@usuhs.edu.
authors.forename: Yifan
authors.initials: Y
authors.lastname: Chen
authors.affiliation: Department of Military and Emergency Medicine, Uniformed Services University of the Health Sciences, Bethesda, MD, USA.
authors.forename: Aminul
authors.initials: A
authors.lastname: Islam
authors.affiliation: Department of Military and Emergency Medicine, Uniformed Services University of the Health Sciences, Bethesda, MD, USA.
authors.forename: Preetha
authors.initials: P
authors.lastname: Abraham
authors.affiliation: Department of Military and Emergency Medicine, Uniformed Services University of the Health Sciences, Bethesda, MD, USA.
authors.forename: Patricia
authors.initials: P
authors.lastname: Deuster
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D000975:Antioxidants / Q000378:metabolism / Q000494:pharmacology*; D015237:Dinoprost / Q000031:analogs & derivatives / Q000097:blood; D005978:Glutathione / Q000097:blood; D050884:HSP72 Heat-Shock Proteins / Q000378:metabolism; D006360:Heat-Shock Proteins / Q000378:metabolism*; D018869:Heat-Shock Response / Q000187:drug effects*; D006358:Hot Temperature; D006979:Hyperthermia, Induced; D007249:Inflammation / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D008099:Liver / Q000378:metabolism; D008297:Male; D008810:Mice, Inbred C57BL; D018482:Muscle, Skeletal / Q000378:metabolism; D009206:Myocardium / Q000378:metabolism; D010084:Oxidation-Reduction; D018384:Oxidative Stress / Q000187:drug effects; D011794:Quercetin / Q000494:pharmacology*; D013482:Superoxide Dismutase / Q000097:blood
chemical_list: D000893:Anti-Inflammatory Agents; D000975:Antioxidants; D050884:HSP72 Heat-Shock Proteins; D006360:Heat-Shock Proteins; D015850:Interleukin-6; C075750:8-epi-prostaglandin F2alpha; D011794:Quercetin; D015237:Dinoprost; D013482:Superoxide Dismutase; D005978:Glutathione
keywords: Cytokine; Flavonoid; Hyperthermia; Mice; SOD; Skeletal muscle