ABSTRACT
<p><b>OBJECTIVE</b>To investigate the inhibitory effect of tetramethylpyrazine (Tet) preconditioning on overload training-induced myocardial apoptosis in rats, and to explore cardioprotective mechanisms of Tet preconditioning.</p><p><b>METHODS</b>A total of 25 male Sprague-Dawley rats were randomly divided into three groups, including the control group (n=5), the overload training group (overload training for 8 weeks, n=10), and the Tet preconditioning group (Tet preconditioning for 8 weeks before overload training, n=10). After 8 weeks, cardiac structure and myocardial apoptosis were analyzed by histology, transmission electron microscopy, and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling assay staining. The expressions of Bcl-2, Bax, Caspase-3, and Caspase-9 in myocardium were evaluated by immunohistochemical staining.</p><p><b>RESULTS</b>Overload training caused swelling, disorder, partial rupture, and necrosis of myocardial focal necrotic fibers, as well as mitochondrial vacuolization, cristae rupturing, and blurring. In contrast, Tet preconditioning attenuated the swelling of myocardial fibers, decreased the amount of ruptured fibers, and inhibited mitochondrial vacuolization, resulting in clear cristae. Overload training significantly increased Bax expression and decreased Bcl-2/Bax ratio when compared with the control group (P<0.01). Conversely, Tet preconditioning significantly increased Bcl-2 expression and the Bcl-2/Bax ratio as compared with the overload training group (P<0.05). Overload training dramatically increased the expressions of Caspase-3 and Caspase-9 when compared with the control groupP<0.05). Following Tet preconditioning, the expression of Caspase-3 was significantly reduced compared with the overload training group (P<0.05), while Caspase-9 expression showed a slight decline (P>0.05).</p><p><b>CONCLUSION</b>Tet preconditioning increased the expression of Bcl-2 and reduced the expression of Caspase-3, thereby attenuating overload training-induced myocardial apoptosis, protecting against overload training-induced myocardial injury, and reducing damage to the myocardium due to overload training.</p>