Rosuvastatin increases myocardial microvessels in SHR rats. Role of thioredoxin-1 and peroxiredoxin-2 expression

Abstract

Beyond their lipid-lowering action, rosuvastatin possesses pleiotropic effects including anti-inflammatory, pro-angiogenic, antioxidant effects and protective actions against endothelial dysfunction [1,2]. The spontaneously hypertensive rats (SHR) have been extensively studied as a model of essential hypertension. Analogous to that seen in humans, prolonged periods of hypertension produce left ventricular (LV) remodeling, hypertrophy and oxidative stress. Thioredoxin (Trx) and peroxiredoxin (Prx) are a ubiquitous family of cysteine-dependent antioxidant proteins, present in mammalian cells including the heart. Several reports exist in the literature indicating that these proteins are induced by oxidative stress [3]. We investigated the possible effect of long-term monotherapy with rosuvastatin in myocardial expression of redoxins and vascular endothelial growth factor (VEGF), and their relations with LV remodeling in adult SHR. Eight-week-old male SHR and Wistar-Kyoto (WKY) rats, were divided into three groups: SHR (n = 20), SHR-R (n = 20; rosuvastatin 10 mg/kg/day) and WKY (n = 20).