2115 HEME OXYGENASE-1 IS INDUCED BY THYROID HORMONE AND INVOLVED IN THYROID HORMONE PRECONDITIONING-INDUCED PROTECTION AGAINST RENAL WARM ISCHEMIA IN VIVO

You have accessJournal of UrologyTransplantation & Vascular Surgery: Renal Transplantation, Renal Vascular Surgery1 Apr 20132115 HEME OXYGENASE-1 IS INDUCED BY THYROID HORMONE AND INVOLVED IN THYROID HORMONE PRECONDITIONING-INDUCED PROTECTION AGAINST RENAL WARM ISCHEMIA IN VIVO ZhongXing Zhou, ShuYan Lu, LI Zuo, and JianGang Zou ZhongXing ZhouZhongXing Zhou Changzhou, China, People's Republic of More articles by this author , ShuYan LuShuYan Lu Changzhou, China, People's Republic of More articles by this author , LI ZuoLI Zuo Changzhou, China, People's Republic of More articles by this author , and JianGang ZouJianGang Zou Changzhou, China, People's Republic of More articles by this author View All Author Informationhttps://doi.org/10.1016/j.juro.2013.02.2024AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookTwitterLinked InEmail INTRODUCTION AND OBJECTIVES To investigated the effect of thyroid hormone on HO-1 expression and the possible relation between HO-1 and the thyroid hormone induced renal protection. METHODS Animals were divided into two different treatment schedules: schedule I was designed to evaluate the effects of a single injection of T3 on HO-1 expression and the relationship between T3-induced oxidative stress and HO-1 expression by assessment of parameters related to serum FT3 level, renal oxidative stress, HO-1 expression and renal function for up to 72 h after treatment. Schedule II was designed to evaluate the participation of HO-1 in thyroid hormone pretreatment-induced renal protection against ischemia rperfusion injury. T3 (0.1 mg/kg body weight) and equivalent volumes of hormone vehicle (normal saline) were injected intraperitoneally (i.p.) to rats and studies were performed at the indicated times after treatment.Plasma 3,5,3`-triiodothyronine quantitative assessment was performed with radioimmunoassay. Oxidative stress was detected by assessment of reduced glutathione equivalents and malondialdehyde concentration. The assessment of Serum creatinine and urea nitrogen was performed. Histological examination, transmission electron microscopic examination and western blotting analysis, RT-PCR were used. RESULTS T3 administration in rat kidneys induced HO-1 expression in a time-dependent and dose-dependent way, and its expression was accompanied with significant depletion of reduced glutathione and increase in malondialdehyde content, showing a moderate oxidative stress that turns to normal level 48 h after drug injection. Thyroid hormone pretreatment (10 μg/100 g body weight) 48 h before IR procedure significantly decreased serum creatinine and urea nitrogen and preserved renal histology, with significant reduction of parameters about oxidative stress and over-expression of HO-1 compared with that of IR group. CONCLUSIONS The results of this study indicate that T3 upregulate HO-1 expression accompanied with transient induction of oxidative stress and/or nitrositive stress and its overexpression by T3 leads to significant prevention of renal injury associated with IR. This cytopretection may be ascribed to the antioxidant function of HO-1 to re-establish redox homeostasis after renal IRI, although other protective actions of HO-1 cannot be discarded. © 2013 by American Urological Association Education and Research, Inc.FiguresReferencesRelatedDetails Volume 189Issue 4SApril 2013Page: e866-e867 Advertisement Copyright & Permissions© 2013 by American Urological Association Education and Research, Inc.MetricsAuthor Information ZhongXing Zhou Changzhou, China, People's Republic of More articles by this author ShuYan Lu Changzhou, China, People's Republic of More articles by this author LI Zuo Changzhou, China, People's Republic of More articles by this author JianGang Zou Changzhou, China, People's Republic of More articles by this author Expand All Advertisement Advertisement PDF downloadLoading ...