Denipote Fabiana, Ardisson Lidiane P, Azevedo Paula S, Minicucci Marcos F, Lima-Leopoldo Ana P, Chiuso-Minicucci Fernanda, Polegato Bertha F, Matsubara Beatriz B, Matsubara Luiz S, Novelli Ethel, Paiva Sergio A R, Zornoff Leonardo A M
Internal Medicine Department, Botucatu Medical School, Univ Estadual Paulista, Botucatu, Brazil.
Cell Physiol Biochem. 2011;27(3-4):291-8. doi: 10.1159/000327955. Epub 2011 Apr 1.
BACKGROUND/AIMS: To investigate the effect of taurine on cardiac remodeling induced by smoking.
In the first step, rats were allocated into two groups: Group C (n = 14): control; Group T (n = 14): treated with taurine (3% in drinking water), for three months. In the second step, rats were allocated into two groups: Group ETS (n = 9): rats exposed to tobacco smoke; Group ETS-T (n = 9): rats exposed to tobacco smoke and treated with taurine for two months.
After three months, taurine presented no effects on morphological or functional variables of normal rats assessed by echocardiogram. On the other hand, after two months, ETS-T group presented higher LV wall thickness (ETS = 1.30 (1.20-1.42); ETS-T = 1.50 (1.40-1.50); p = 0.029), E/A ratio (ETS = 1.13 ± 0.13; ETS-T = 1.37 ± 0.26; p = 0.028), and isovolumetric relaxation time normalized for heart rate (ETS = 53.9 ± 4.33; ETS-T = 72.5 ± 12.0; p < 0.001). The cardiac activity of the lactate dehydrogenase was higher in the ETS-T group (ETS = 204 ± 14 nmol/mg protein; ETS-T = 232 ± 12 nmol/mg protein; p < 0.001). ETS-T group presented lower levels of phospholamban (ETS = 1.00 ± 0.13; ETS-T = 0.82 ± 0.06; p = 0.026), phosphorylated phospholamban at Ser16 (ETS = 1.00 ± 0.14;ETS-T = 0.63 ± 0.10;p = 0.003), and phosphorylated phosfolamban/phospholamban ratio (ETS = 1.01 ± 0.17; ETS-T = 0.77 ± 0.11; p = 0.050).
In normal rats, taurine produces no effects on cardiac morphological or functional variables. On the other hand, in rats exposed to cigarette smoke, taurine supplementation increases wall thickness and worsens diastolic function, associated with alterations in calcium handling protein and cardiac energy metabolism.
背景/目的：研究牛磺酸对吸烟所致心脏重塑的影响。
第一步，将大鼠分为两组：C组（n = 14）：对照组；T组（n = 14）：饮用含3%牛磺酸的水，为期三个月。第二步，将大鼠分为两组：ETS组（n = 9）：暴露于烟草烟雾的大鼠；ETS-T组（n = 9）：暴露于烟草烟雾并接受牛磺酸治疗两个月的大鼠。
三个月后，通过超声心动图评估，牛磺酸对正常大鼠的形态学或功能变量无影响。另一方面，两个月后，ETS-T组的左心室壁厚度更高（ETS组 = 1.30（1.20 - 1.42）；ETS-T组 = 1.50（1.40 - 1.50）；p = 0.029），E/A比值更高（ETS组 = 1.13 ± 0.13；ETS-T组 = 1.37 ± 0.26；p = 0.028），心率校正后的等容舒张时间更长（ETS组 = 53.9 ± 4.33；ETS-T组 = 72.5 ± 12.0；p < 0.001）。ETS-T组的乳酸脱氢酶心脏活性更高（ETS组 = 204 ± 14 nmol/mg蛋白；ETS-T组 = 232 ± 12 nmol/mg蛋白；p < 0.001）。ETS-T组的受磷蛋白水平更低（ETS组 = 1.00 ± 0.13；ETS-T组 = 0.82 ± 0.06；p = 0.026），丝氨酸16位点的磷酸化受磷蛋白水平更低（ETS组 = 1.00 ± 0.14；ETS-T组 = 0.63 ± 0.10；p = 0.003），磷酸化受磷蛋白/受磷蛋白比值更低（ETS组 = 1.01 ± 0.17；ETS-T组 = 0.77 ± 0.11；p = 0.050）。
在正常大鼠中，牛磺酸对心脏形态学或功能变量无影响。另一方面，在暴露于香烟烟雾的大鼠中，补充牛磺酸会增加心室壁厚度并使舒张功能恶化，这与钙处理蛋白和心脏能量代谢的改变有关。
