Heme Oxygenase-1 Prevents Hyperthyroidism Induced Hepatic Damage via an Antioxidant and Antiapoptotic Pathway

被引：23

作者：

Giris, Murat ^{[2
]}

Erbil, Yesim ^{[1
]}

Depboylu, Bilge ^{[2
]}

Mete, Ozgur ^{[3
]}

Turkoglu, Umit ^{[2
]}

Abbasoglu, Semra Dogru ^{[2
]}

Uysal, Mujdat ^{[2
]}

机构：

[1] Istanbul Univ, Istanbul Fac Med, Dept Gen Surg, TR-34093 Istanbul, Turkey

[2] Istanbul Univ, Istanbul Fac Med, Dept Biochem, TR-34093 Istanbul, Turkey

[3] Istanbul Univ, Istanbul Fac Med, Dept Pathol, TR-34093 Istanbul, Turkey

来源：

JOURNAL OF SURGICAL RESEARCH | 2010年 / 164卷 / 02期

关键词：

heme oxygenase; apoptosis; hyperthyroidism; liver damage; THYROID-HORMONES; RAT-LIVER; GLUTAMINE PROTECTS; OXIDATIVE STRESS; HO-1; INDUCTION; MITOCHONDRIA; APOPTOSIS; GLUTATHIONE; DISEASE; DEATH;

D O I：

10.1016/j.jss.2009.04.013

中图分类号：

R61 [外科手术学];

学科分类号：

摘要：

Background The exact pathogenesis of hepatic dysfunction in hyperthyroidism is still unknown We aimed to investigate the pathogenesis of liver dysfunction caused by hyperthyroidism through inducing heme oxygenase-1 (HO-1) expression, which has antioxidant and anti-apoptotic properties Methods Rats were divided into six groups untreated (group 1), treated with zinc protoporphyrin (ZnPP) (group 2), treated with hemin (group 3), treated with tri-iodothyronine (T3) (group 4), treated with T3 and ZnPP (group 5), and treated with T3 and hemin (group 6) After 22 d, oxidative stress and antioxidant enzymes and the expression of HO-1, mitochondrial permeability transition, cytochrome c, Bax, Bcl-2, caspase-3, caspase-8, and caspase-3 activity, and terminal deoxynucleotidyl transferase mediated dUTP nick-end labeling (TUNEL) assay were examined Results Hyperthyroidism induced oxidative stress of liver tissue was ameliorated by HO-1 induction Administration of hemin (HO 1 inducer) increased Bcl-2 expression Decreased expression of cytochrome c was accompanied by a decrease in caspase-3, caspase-8, Bax expression, and caspase 3 activity The apoptotic activity and oxidative damage were found to be increased by the administration of ZnPP (HO-1 inhibitor) Immunohistochemistry findings supported these results Conclusion HO-1 induction plays a protective role in the pathogenesis of the liver dysfunction in hyperthyroidism This effect is dependent on modulation of the antiapoptotic and antioxidative pathways by HO-1 expression (C) 2010 Elsevier Inc All rights reserved

引用

页码：266 / 275

页数：10

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