title: Ischemic postconditioning prevents renal ischemia reperfusion injury through the induction of heat shock proteins in rats.
abstract: Ischemic postconditioning (IPo) attenuates ischemia‑reperfusion injuries (IRI) in various organs, of both animals and humans. This study tested the hypothesis that IPo attenuates renal IRI through the upregulation of heat shock protein (HSP)70, HSP27 and heme oxygenase‑1 (HO‑1, also known as HSP 32) expression. Adult Sprague Dawley rats were subjected to bilateral renal ischemia for 45 min followed by reperfusion for up to 48 h. One group of rats received IPo prior to restoring full perfusion. Another group was administered 100 mg/kg HSP inhibitor quercetin, injected intraperitoneally 1 h prior to ischemia. Control rats received sham operations. Renal IR resulted in severe morphological and pathological changes, with increased serum creatinine and blood urea nitrogen concentrations. IR resulted in increased inflammation by inducing plasma tumor necrosis factor‑α and renal nuclear factor kappa‑light‑chain‑enhancer of activated B cells expression. IR also increased lipid peroxidation, as indicated by elevated malondialdehyde content, reduced superoxide dismutase activity and increased renal apoptosis. Renal HSP70, HSP27 and HO‑1 mRNA and protein levels were increased by IR and further elevated by IPo. IPo attenuated these changes observed in pathology, lipid peroxidation, apoptosis and inflammation. Quercetin treatment abolished all the protective effects of IPo. In conclusion, this study showed that IPo can attenuate lipid peroxidation, apoptosis and inflammation as well as renal IRI by upregulating the expression of HSP70, HSP27 and HO‑1.
authors.affiliation: Department of Anesthesiology, Hebei General Hospital, Shijiazhuang, Hebei 050051, P.R. China.
authors.forename: Qiongmei
authors.initials: Q
authors.lastname: Guo
authors.affiliation: Department of Anesthesiology, Xingtai Eye Hospital, Xingtai, Hebei 054001, P.R. China.
authors.forename: Xuefang
authors.initials: X
authors.lastname: Du
authors.affiliation: Department of Anesthesiology, Hebei General Hospital, Shijiazhuang, Hebei 050051, P.R. China.
authors.forename: Yanli
authors.initials: Y
authors.lastname: Zhao
authors.affiliation: Department of Anesthesiology, Hebei General Hospital, Shijiazhuang, Hebei 050051, P.R. China.
authors.forename: Dong
authors.initials: D
authors.lastname: Zhang
authors.affiliation: Department of Anesthesiology, Hebei General Hospital, Shijiazhuang, Hebei 050051, P.R. China.
authors.forename: Lihui
authors.initials: L
authors.lastname: Yue
authors.affiliation: Department of Urinary Surgery, Hebei General Hospital, Shijiazhuang, Hebei 050051, P.R. China.
authors.forename: Zhenxian
authors.initials: Z
authors.lastname: Wang
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000502:physiology; D055551:HSP27 Heat-Shock Proteins / Q000378:metabolism*; D018840:HSP70 Heat-Shock Proteins / Q000378:metabolism*; D051547:Heme Oxygenase-1 / Q000378:metabolism; D057775:Ischemic Postconditioning / Q000379:methods; D007668:Kidney / Q000378:metabolism*; D015227:Lipid Peroxidation / Q000502:physiology; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000378:metabolism*
chemical_list: D055551:HSP27 Heat-Shock Proteins; D018840:HSP70 Heat-Shock Proteins; D008315:Malondialdehyde; D051547:Heme Oxygenase-1