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Redox Regulation of Myocardial Erk 1/2 Phosphorylation in Experimental Hyperthyroidism Role of Thioredoxin-Peroxiredoxin System
- Source :
- Journal of Cardiovascular Pharmacology; November 2010, Vol. 56 Issue: 5 p513-517, 5p
- Publication Year :
- 2010
-
Abstract
- 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−1subcutaneously, 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 T4group. 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.
Details
- Language :
- English
- ISSN :
- 01602446 and 15334023
- Volume :
- 56
- Issue :
- 5
- Database :
- Supplemental Index
- Journal :
- Journal of Cardiovascular Pharmacology
- Publication Type :
- Periodical
- Accession number :
- ejs49052382
- Full Text :
- https://doi.org/10.1097/FJC.0b013e3181f50a70