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Taurine attenuates cardiac remodeling after myocardial infarction

2013; Elsevier BV; Volume: 168; Issue: 5 Linguagem: Inglês

10.1016/j.ijcard.2013.07.091

1874-1754

Lidiane P. Ardisson, Bruna Paola Murino Rafacho, Dos Santos, Heloísa Balan Assalin, Andréa Gonçalves, Paula S. Azevedo, Marcos Ferreira Minicucci, Bertha Furlan Polegato, Katashi Okoshi, Júlio Sérgio Marchini, Luı́s Fernando Barbisan, Ana Angélica Henrique Fernandes, Fábio Rodrigues Ferreira Seiva, Sérgio Alberto Rupp de Paiva, Leonardo A. M. Zornoff,

Cardiovascular Function and Risk Factors

After myocardial infarction, cardiac remodeling is associated with progressive ventricular dysfunction and cardiovascular death [[1]Zornoff L.A. Paiva S.A. Duarte D.R. Spadaro J. Ventricular remodeling after myocardial infarction: concepts and clinical implications.Arq Bras Cardiol. 2009; 92: 157-164Crossref PubMed Scopus (78) Google Scholar]. Therefore, the objective of this study was to investigate the effect of taurine on cardiac remodeling induced by myocardial infarction in rats. All experiments were approved by the Animal Ethics Committee of our institution. The authors of this manuscript have certified that they comply with the Principles of Ethical Publishing in the International Journal of Cardiology. Male Wistar rats weighing 200–250 g were allocated into the following three groups: Group C (n = 10): the rats were submitted to surgery, but they did not undergo coronary occlusion; Group MI (n = 31): the rats were submitted to coronary occlusion; Group MI-T (n = 30): the rats were submitted to coronary occlusion and treated with taurine (3% in drinking water). The dose of taurine and route of administration have been shown to modulate cardiac remodeling [[2]Denipote F. Ardisson L.P. Azevedo P.S. et al.Influence of taurine on cardiac remodeling induced by tobacco smoke exposure.Cell Physiol Biochem. 2011; 27: 291-298Crossref PubMed Scopus (15) Google Scholar]. The methods were performed as previously described [2Denipote F. Ardisson L.P. Azevedo P.S. et al.Influence of taurine on cardiac remodeling induced by tobacco smoke exposure.Cell Physiol Biochem. 2011; 27: 291-298Crossref PubMed Scopus (15) Google Scholar, 3Minicucci M.F. Azevedo P.S. Martinez P.F. et al.Critical infarct size to induce ventricular remodeling, cardiac dysfunction and heart failure in rats.Int J Cardiol. 2011; 151: 242-243Abstract Full Text Full Text PDF PubMed Scopus (28) Google Scholar, 4Paiva S.A. Novo R. Matsubara B.B. et al.β-Carotene attenuates the paradoxical effect of tobacco smoke on the mortality of rats after experimental myocardial infarction.J Nutr. 2005; 135: 2109-3113PubMed Google Scholar, 5Ardisson L.P. Minicucci M.F. Azevedo P.S. et al.Influence of AIN-93 diet on mortality and cardiac remodeling after myocardial infarction in rats.Int J Cardiol. 2012; 156: 265-269Abstract Full Text Full Text PDF PubMed Scopus (11) Google Scholar, 6Azevedo P.S. Minicucci M.F. Chiuso-Minicucci F. et al.Ventricular remodeling induced by tissue vitamin A deficiency in rats.Cell Physiol Biochem. 2010; 26: 395-402Crossref PubMed Scopus (31) Google Scholar, 7Rafacho B.P. Santos P. Assalin H.B. et al.Role of vitamin D in the cardiac remodeling induced by tobacco smoke exposure.Int J Cardiol. 2012; 155: 472-473Abstract Full Text Full Text PDF PubMed Scopus (15) Google Scholar]. Considering our results, the cardiac taurine levels were higher in the MI-T in comparison with the other groups (C = 0.100 ± 0.04 μmol/g, MI = 0.175 ± 0.07 μmol/g, MI-T = 0.419 ± 0.187 μmol/g; p = 0.022). The infarct size was not different among the infarcted groups (MI = 31.3 ± 11.5%, MI-T = 31.7 ± 10.4%). Taurine attenuated the increase in the left atrium, the left ventricular (LV) mass, the LV posterior wall thickness (PWT), and the interventricular septum thickness induced by infarction. With regard to the functional variables, taurine did not improve systolic dysfunction induced by coronary occlusion. On the other hand, taurine attenuated the diastolic dysfunction caused by infarction (Table 1).Table 1Echocardiographic, biochemical and molecular data.VariablesC (n = 6)MI (n = 6)MI-T (n = 6)Caspase 3 (U/cm2 × 103)0.026 ± 0.030.47 ± 0.35⁎p<0.05 versus C.0.11 ± 0.12#p<0.05 versus MI.MMP-2542 (356–723)1250 (1180–1270)⁎p<0.05 versus C.622 (343–964)MMP-9991 (836–1065)3150 (2010–3735)⁎p<0.05 versus C.1190 (1055–1505)LDH (nmol/mg protein)618 ± 128943 ± 1671283 ± 236⁎p<0.05 versus C.OHADH (nmol/mg protein)82 (80–91)182 (129–232)341 (250–419)⁎p<0.05 versus C.CS (nmol/mg protein)384 (336–408)508 (422–563)669 (542–768)⁎p<0.05 versus C.GSH-Px (nmol/mg protein)624 ± 165821 ± 203⁎p<0.05 versus C.494 ± 74#p<0.05 versus MI.Nrf-20.63 ± 0.210.25 ± 0.16⁎p<0.05 versus C.0.42 ± 0.14LA (mm)a(C, n=10; MI, n=21; MI-T, n=22).5.3 ± 0.76.8 ± 1.0⁎p<0.05 versus C.6.1 ± 0.8⁎p<0.05 versus C.#p<0.05 versus MI.PWT (mm)a(C, n=10; MI, n=21; MI-T, n=22).1.4 (1.31–1.46)1.59 (1.53–1.7)⁎p<0.05 versus C.1.5 (1.4–1.6)⁎p<0.05 versus C.#p<0.05 versus MI.IVRT/R-R0.5 (ms)a(C, n=10; MI, n=21; MI-T, n=22).78.5 ± 21.6100 ± 21.3⁎p<0.05 versus C.91.1 ± 19.7C: control animals; MI: infarcted animals; MI-T: infarcted animals supplemented with taurine; MMP: metalloproteinase; LDH: lactate dehydrogenase; OHADH: β-Hydroxyacylcoenzyme A dehydrogenase; CS: citrate synthase; GSH-Px: glutathione peroxidase; Nrf-2: nuclear-factor-E2-related factor; LA: left atrium; PWT: left ventricular posterior wall thickness; IVRT/R-R0.5: isovolumetric relaxation time normalized for heart rate. Data are expressed as the mean ± SD or medians (including the lower quartile and upper quartile).a (C, n = 10; MI, n = 21; MI-T, n = 22). p < 0.05 versus C.# p < 0.05 versus MI. Open table in a new tab C: control animals; MI: infarcted animals; MI-T: infarcted animals supplemented with taurine; MMP: metalloproteinase; LDH: lactate dehydrogenase; OHADH: β-Hydroxyacylcoenzyme A dehydrogenase; CS: citrate synthase; GSH-Px: glutathione peroxidase; Nrf-2: nuclear-factor-E2-related factor; LA: left atrium; PWT: left ventricular posterior wall thickness; IVRT/R-R0.5: isovolumetric relaxation time normalized for heart rate. Data are expressed as the mean ± SD or medians (including the lower quartile and upper quartile). In relation to metalloproteinase (MMP)-2 and -9, the taurine group showed intermediated values between the C and MI groups. The same phenomenon was observed for the Nrf-2 values. In addition, taurine treatment decreased the GSH-Px and caspase-3 levels, in comparison with the MI group. On the other hand, taurine treatment increased the lactate dehydrogenase, β-hydroxyacylcoenzyme A dehydrogenase, and citrate synthase levels in comparison with controls, as shown in Table 1. In conclusion, taurine attenuated morphological and functional variables after three months following coronary occlusion. Importantly, this effect was related to decreased apoptosis, oxidative stress, and MMP-2 and MMP-9 activation and was associated with improved cardiac energy metabolism.