Tribulus teresstris modulates heat shock protein and key anti-apoptotic proteins in the Langendorff model of myocardial ischemia and reperfusion injury

The cardioprotective effects of Tribulus teresstris (Tt), a medicinal herb, used in Indian system of medicine was evaluated in the Langendorff model of myocardial ischemia and reperfusion (I-R) injury. Tt (1, 2.5, 5, 10 mg/kg) was orally fed to healthy experimental rats once a day for 21 days followed by global ischemia and reperfusion injury. Biochemical parameters: lipid peroxidation product thiobarbituric acid reactive substances (TBARS), endogenous antioxidant: glutathione, antioxidant enzymes (superoxide dismutase (SOD), catalase (CAT), glutathione peroxidases (GSHPx)) and myocardial enzyme creatine phosphokinase (CPK) were evaluated. To correlate the biochemical derangement and altered cardiac performance during I-R, changes in the hemodynamic variables heart rate (HR) and coronary perfusion pressure (CPP) was measured. Myocardial apoptotic was quantified using terminal deoxynucleotidyl transferase mediated dUTP nick end labeling (TUNEL) method. The expression of anti-apoptotic protein Bcl-2, pro-apoptotic protein Bax, enzyme: Caspase 3 and heat shock protein (HSP) in cardiac myocytes was detected by immunohistochemistry. As compared with sham group, the CPP, TBARS levels, myocardial apoptosis, expression of Caspase 3, Bax, heat shock protein (HSP 72) proteins were increased significantly in I-R control group. Tt pre-treatment significantly restored the antioxidant network of the myocardium, reduced myocardial apoptosis, Bax, HSP 72 protein expression. These beneficial effects also translated into favourable hemodynamic effects. Histopathological studies and myocardial CPK content further confirmed the cardioprotective effects of Tt (2.5 mg/kg) in the experimental model of I-R injury.