Reactive oxygen species participate in signal transduction during cellular growth and differentiation under hypertensive stress. Although cellular redox balance may play an important role in cardiac hypertrophy and its regression, the mechanisms of regulation of redox are incompletely defined. We analysed the redox status, expressions of redox-regulating protein, thioredoxin (Trx) and peroxiredoxin (Prx) in the heart from pressure overload-induced LV hypertrophy (LVH), and the change of Trx and Prx during LVH regression. LVH was obtained by the controlled constriction of the transverse aorta (TAC) in Spraque–Dawley rats. Dynamic expressions of Trx, thioredoxin-interacting protein (Txnip), endogenous inhibitor of Trx, and thioredoxin reductase (TrxR) were evaluated by Western blot, and also mRNA of Prx-1, 2, 3, 4, 5 were evaluated by polymerase chain reaction in hearts obtained at 1, 3, 5, 7, 14 days after TAC and 1, 3, 5, 7, 14 days after relieving TAC for LVH regression (two rats at each time point). Systolic BP was significantly increased immediately after TAC and persisted up to 2 weeks (195.0 ± 5.0 vs. 110.9 ± 10.2 mmHg, p < 0.01). Septal wall thickness (1.94 ± 0.38 vs. 1.28 ± 0.13 mm) and LV weight/body weight ratio (2.69 ± 0.31 vs. 2.26 ± 0.28 mg/g) was significantly increased at 2 weeks after TAC compared to baseline (p < 0.05). Expression of Trx/Txnip ratio and Prx-1, 2, 3, 4, 5 was significantly increased during acutely hypertensive stress period (days 1–5) and then gradually decreased during relatively adaptive period (up to day 14). However, mRNA expression of TrxR was increased up to 7 days after TAC. Systolic BP and LV mass was significantly decreased after relieving TAC. Immediately after LV unloading, the expression pattern of Trx and Txnip was reversed. Increased mRNA expression of Prx-1, 2, 3, 4, 5 at day 1 after relieving TAC gradually declined until day 14. Taken together, Trx and Prx may play a crucial role in the development and regression of hypertension and LVH.
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© 2007 Published by Elsevier Inc.