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.Keywords: Sodium Aescinate, Methyl Parathion, Acute Organophosphorus Pesticide Poisoning, Myocardial Injury
Highlights
Acute organophosphorus pesticide poisoning (AOPP) is a disease caused by organophosphorus pesticide abuse or accidental poisoning with a high mortality especially in rural regions [1]
Researchers found that pesticides induce oxidative stress, causing DNA damage and apoptosis in myocardial cells; these effects may constitute the mechanism of methyl parathion (MP)-induced myocardial injury [5]
The western blotting results revealed that in MP group, the expression of cleaved caspase 3 and Bax increased while Bcl-2 decreased (Figure 4B).Sodium aescinate treatment decreased the expression of cleaved caspase 3 and Bax but increased Bcl-2 in a dose-dependent manner
Summary
Acute organophosphorus pesticide poisoning (AOPP) is a disease caused by organophosphorus pesticide abuse or accidental poisoning with a high mortality especially in rural regions [1]. AOPP often results from the accumulation of Ach within synapses of the central and peripheral Cardiac complications, such as various arrhythmias, dysarteriotony, and myocardial damage, are major causes of death after AOPP [4]. The kits for MDA (A003-1), SOD, GSH-px, and GSH were obtained from Nanjing Jiancheng Bioengineering Research Institute (Nanjing, China). Peripheral blood was collected in heparin-treated tubes by and centrifuged to obtain plasma for further analysis. Blood samples were collected in tubes pretreated with anticoagulant (aprotinin for ANP, heparin for cTnT) and centrifuged (3000 g at 4 °C for 10 min) to obtain plasma for further analysis. The supernatant was collected for further analysis of MDA, SOD, GSH-px, and GSH using assay kits purchased from Nanjing Jincheng Corp, China. Sprague-Dawley rats were obtained from Vital River Laboratory Animal Technology (Beijing, China). The proteins were detected using a chemiluminescence imaging machine and analyzed with the NIH Image J software
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