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

G CAO; GÓMEZ LLAMBÍ H; MULLER A; G OTTAVIANO; J MILEI

INTERNATIONAL JOURNAL OF CARDIOLOGY

ELSEVIER IRELAND LTD

Lugar: Ireland; Año: 2014 vol. 174 p. 153 - 155

0167-5273

delay early vascular healing [11], the causes of ST and MI aremultifactorial and the precise reasons for these conflict findingsremain to be established.Appendix A. Supplementary dataSupplementary data to this article can be found online at http://dx.doi.org/10.1016/j.ijcard.2014.03.167.References[1] McFadden EP, Stabile E, Regar E, et al. Late thrombosis in drug-eluting coronarystents after discontinuation of antiplatelet therapy. Lancet 2004;364:1519?21.[2] Palmerini T, Biondi-Zoccai G, Della RD, et al. Stent thrombosis with drug-elutingand bare-metal stents: evidence from a comprehensive network meta-analysis.Lancet 2012;379:1393?402.[3] Chevalier B, Serruys PW, Silber S, et al. Randomised comparison of NOBORI,biolimus A9-eluting coronary stent with a Taxus(R), paclitaxel-eluting coronarystent in patients with stenosis in native coronary arteries: the NOBORI 1 trial.EuroIntervention 2007;2:426?34.[4] Smits PC, Hofma S, Togni M, et al. 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Int J Cardiol 2013;168:4617?23.http://dx.doi.org/10.1016/j.ijcard.2014.03.1670167-5273/© 2014 Elsevier Ireland Ltd. All rights reserved.Rosuvastatin increases myocardial microvessels in SHR rats.Role of thioredoxin-1 and peroxiredoxin-2 expression☆Gabriel Cao ⁎,1, Hernán Gómez Llambí 1, Angélica Muller 1, Graciela Ottaviano 1, José Milei 1Instituto de Investigaciones Cardiológicas ?Prof. Dr. Alberto C. Taquini? (ININCA), University of Buenos Aires ? CONICET, Buenos Aires, Argentinaa r t i c l e i n f oArticle history:Received 25 January 2014Accepted 23 March 2014Available online 28 March 2014Keywords:RosuvastatinSpontaneously hypertensive ratHeartAntioxidant effectBeyond their lipid-lowering action, rosuvastatin possesses pleiotropiceffects including anti-inflammatory, pro-angiogenic, antioxidanteffects and protective actions against endothelial dysfunction [1,2].The spontaneously hypertensive rats (SHR) have been extensivelystudied as a model of essential hypertension. Analogous to that seenin humans, prolonged periods of hypertension produce leftventricular (LV) remodeling, hypertrophy and oxidative stress.Thioredoxin (Trx) and peroxiredoxin (Prx) are a ubiquitous familyof cysteine-dependent antioxidant proteins, present in mammaliancells including the heart. Several reports exist in the literatureindicating that these proteins are induced by oxidative stress [3]. Weinvestigated the possible effect of long-term monotherapy withrosuvastatin in myocardial expression of redoxins and vascularendothelial growth factor (VEGF), and their relations with LVremodeling 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). For16 months, animals were housed in individual cages and were given☆ This work was supported by the National Scientific and Technical Research CouncilPIP No. 112-2000801-03167, Argentina (CONICET).⁎ Corresponding author at: Instituto de Investigaciones Cardiológicas ?Prof. Dr.Alberto C. Taquini? (ININCA), University of Buenos Aires ?CONICET, Marcelo T de Alvear2270, C1122AAJ Buenos Aires, Argentina.E-mail address: gabrielcao@fibertel.com.ar (G. Cao).1 This author takes responsibility for all aspects of the reliability and freedom frombias of the data presented and their discussed interpretation.Table 1Body weight, left ventricular mass, systolic blood pressure, stereological andimmunohistochemical parameters in the experimental groups.