Effect of sodium aescinate on methyl parathion-induced myocardial injury in rats

Abstract

Purpose: To explore the effects and mechanism of sodium aescinate (SA) on methyl parathion (MP)-induced myocardial injury. Methods: Rats were divided into following groups: In Control group, rats were administered 0.9 % NaCl by intraperitoneal injection. In MP group, rats were administered 20 mg/kg MP by intraperitoneal injection. In MP + SA group, rats were administered 20 mg/kg MP in combination with SA at a concentration of 0.5, 1.0, or 1.5 mg/kg by intraperitoneal injection. Histological changes were assessed by H&E staining. Serum levels of cardiac troponin T (CTnT) and atrial natriuretie peptide (ANP) were measured by automatic biochemical analyzer and real-time polymerase chain reaction (RT-PCR), respectively. The levels of malondiadehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and glutathione (GSH) in heart tissue was detected by spectrophotometry. The apoptosis of myocardial cells was measured by the terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) assay. The level of apoptosis-related proteins was assessed by western blot. Results: Superoxide dismutase attenuated MP-induced myocardial injury, and decreased the levels of ANP and cTnT in serum (p < 0.01). Superoxide dismutase attenuated the MP-induced decrease in GSH, GSH-px, and SOD expression (p < 0.05) but increased MDA level (p < 0.01). Moreover, SA inhibited the apoptosis of myocardial cells and regulation of apoptosis-related protein expression (e.g., Bax, Bcl-2, and caspase 3). Conclusion: These results demonstrate that SA attenuates MP-induced myocardial injury by regulating oxidative stress and apoptosis.