过氧化物还原蛋白
激酶
硫氧还蛋白
MAPK/ERK通路
内科学
内分泌学
谷胱甘肽过氧化物酶
谷胱甘肽
抗氧化剂
细胞外
化学
氧化应激
p38丝裂原活化蛋白激酶
医学
过氧化物酶
生物化学
酶
超氧化物歧化酶
作者
Alex Sander da Rosa Araújo,Tânia Regina Gattelli Fernandes,Maria Flávia Marques Ribeiro,Neelam Khaper,Adriane Belló‐Klein
出处
期刊:Journal of Cardiovascular Pharmacology
[Ovid Technologies (Wolters Kluwer)]
日期:2010-11-01
卷期号:56 (5): 513-517
被引量:17
标识
DOI:10.1097/fjc.0b013e3181f50a70
摘要
The present study was conducted to test whether adaptation in the antioxidant system would differentially modulate prosurvival and proapoptotic proteins in hyperthyroidism-induced cardiac hypertrophy. Male Wistar rats were divided into 4 groups: control, vitamin E (20 mg·kg−1·d−1 subcutaneously, 28 days), thyroxine (T4) (12 mg/L in drinking water for 28 days), and T4 + vitamin E. Cardiac mass, redox ratio, glutathione peroxidase (GPx) and glutathione reductase (GR) activities, NF-E2-related factor 2 (Nrf2) thioredoxin-1 (Trx-1), peroxiredoxin-6 (Prx-6), phospho-extracellular-signal-regulated kinases 1/2 (p-ERK 1/2)/extracellular-signal-regulated kinases 1/2 (ERK1/2), and phospho-c-Jun N-terminal kinase (p-JNK)/c-Jun N-terminal kinase (JNK) myocardial protein expression were quantified. Cardiac hypertrophy was attenuated in the T4 + vitamin E group. The redox ratio; GPx and GR; as well as Nrf2, Trx-1, Prx-6, and p-ERK1/2/ERK1/2 immunocontent were elevated in T4 group. All these effects were attenuated by vitamin E administration. p-JNK/JNK remained unchanged in all the groups. The overall results suggest that redox imbalance due to hyperthyroidism induce adaptation of antioxidant systems, favoring ERK1/2 activation and leading to development of cardiac hypertrophy.
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