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Heme oxygenase-1 is induced by thyroid hormone and involved in thyroid hormone preconditioning-induced protection against renal warm ischemia in rat.

Abstract：

: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).

journal_name

Mol Cell Endocrinol

journal_title

Molecular and cellular endocrinology

authors

Li F,Lu S,Zhu R,Zhou Z,Ma L,Cai L,Liu Z

doi

10.1016/j.mce.2011.03.019

subject

Has Abstract

pub_date

2011-06-06 00:00:00

pages

54-62

issue

1-2

eissn

0303-7207

issn

1872-8057

pii

S0303-7207(11)00179-1

journal_volume

339

pub_type

杂志文章

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