Attenuative role of didymin against paraquat prompted cardiotoxicity in albino rats

Abstract

Paraquat (PQ) an herbicide that is commonly used to remove undesirable grasses. However, PQ also causes cardiac damage through reactive oxygen species (ROS) production. Didymin (DYD) is a dietary flavone, present in citrus fruits and campanula. DYD displays multiple therapeutic activities i.e., anti-oxidant, hepatoprotective, neuroprotective and free radical salvaging. Therefore, the present study was planned to explore the ameliorative effect of DYD against PQ instigated cardiac damage. 24 rats were separated into 4 groups, control, PQ administered PQ + DYD co-administered orally and DYD only administered group. PQ intoxication significantly reduced anti-oxidants including (SOD, GST, GSH, CAT, GPx and GSR activities, while increasing malondialdehyde (MDA) and ROS levels. PQ intoxication escalated the level of cardiac injury marker i.e., creatine kinase myoglobin binding (CK-MB), troponin, creatinine phosphokinase (CPK) and lactate dehydrogenase (LDH). PQ also augmented inflammatory markers i.e., (TNF-α, IL-1β, NF-κB, IL-6 levels and COX-2 activity). Moreover, PQ intoxication escalated the apoptotic proteins levels (Bax, Caspase-3 and Caspase-9), while decreasing Bcl-2 level. PQ intoxication also prompted histomorphological anomalies in the heart of rats. Conversely, DYD therapy restored all the anomalies and structural abnormalities owing to its cardioprotective potentials.

Keywords

• Paraquat
• Didymin
• Cardiac damage
• Apoptosis
• Anti-oxidant
• Inflammation