内分泌学
氧化应激
甲状腺
内科学
激素
血红素加氧酶
丙二醛
肾
谷胱甘肽
肌酐
肾缺血
化学
医学
缺血
血红素
再灌注损伤
生物化学
酶
作者
Fēi Li,Shannon Lu,Ruixia Zhu,Zhongxin Zhou,Lingdi Ma,Leiming Cai,Zhiyuan Liu
标识
DOI:10.1016/j.mce.2011.03.019
摘要
Thyroid hormone pretreatment was indicated to increase tissue tolerance to ischemia-reperfusion injury (IRI) in various organs, but the underlying molecular mechanisms remains largely unknown. Induction of heme oxygenase-1 (HO-1) protects organs against IRI. The present study investigated the effect of thyroid hormone on HO-1 expression and the possible relation between HO-1 and the thyroid hormone induced renal protection. T(3) 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/100g 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. In conclusion, T(3) administration involving oxidative stress in kidney exerts significant enhancement of HO-1 expression which may, at least in part, account for the renal preconditioning induced by T(3).
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