Pachypodol attenuates arsenic triggered cardiac damage via rectifying oxidative stress, inflammation, apoptosis and histopathological alterations

Abstract

Arsenic is a lethal toxicant found ubiquitously in the ecosystem which adversely affects the body organs including the heart. Pachypodol (PCHP) is a natural flavone which exhibits substantial pharmacotherapeutic potentials. The rats (n = 24) were distributed into 4 different groups i.e., control, arsenic-intoxicated group (50 mg/kg), arsenic + PCHP-supplemented group (50 mg/kg + 10 mg/kg) & PCHP-treated (10 mg/kg) group. It was assessed that arsenic administration subsided catalase (CAT), glutathione reductase (GSR), superoxide dismutase (SOD), glutathione peroxidase (GPx), & glutathione S-transferases (GST) activities while augmenting the levels of reactive oxygen species (ROS) and malondialdehyde (MDA). Furthermore, arsenic exposure increased the levels of cardiac injury markers such as creatine phosphokinase (CPK), creatine kinase-MB (CK-MB), troponin I & lactate dehydrogenase (LDH). Besides, the levels of inflammatory markers nuclear factor kappa B (NF-κB), interleukin-1β (IL-1β), Tumor necrosis factor α (TNF-α), Interleukin 6 (IL-6) levels and cyclooxygenase 2 (COX-2) activity were increased following the arsenic exposure. Similarly, Caspase-3, Bax and Caspase-9 levels were upsurged whereas Bcl-2 level was reduced after arsenic intoxication. In addition, the histopathological assessment revealed a substantial cardiac tissues impairment in the arsenic exposed group. Nonetheless, PCHP supplementation substantially (p < 0.05) recovered the abovementioned arsenic −induced impairments owing to its anti-inflammatory, antioxidative and anti-apoptotic abilities. Therefore, the current research revealed that PCHP might be a promising ameliorative agent to cure arsenic instigated cardiac damages.

Keywords

• Pachypodol
• Arsenic
• Cardiac toxicity
• Oxidative stress
• Inflammation