Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8477803 | Molecular and Cellular Endocrinology | 2011 | 9 Pages |
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. 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. In conclusion, T3 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 T3.
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Authors
Fei Li, Shuyan Lu, Ruixia Zhu, Zhongxin Zhou, Lingdi Ma, Leiming Cai, Zhiyuan Liu,