The Therapeutic Potential of Pelargonidin against Perflourooctane Sulfonate Instigated Cardiac Toxicity via Modulating Nrf-2/Keap-1 Pathway, Inflammatory, Apoptotic and Histological Profile

Perfluorooctane sulfonate (PFOS) is a synthetic chemical that bioaccumulates extensively and persists in the environment, posing significant toxicological risks to human health. Pelargonidin (PLG) is an anthocyanidin that shows various benefits related to health. This investigation was aimed to elucidate the cardioprotective role of PLG in rats subjected to PFOS-induced toxicity. In this experiment, a total of 24 albino rats were distributed into four different groups including, control group, PFOS (10 mg/kg) intoxicated group, PFOS + PLG (10 + 20 mg/kg) co-administered group, and PLG (20 mg/kg) alone treated group. Exposure to PFOS led to suppression of the expressions of Nrf-2 and its related antioxidant genes, while elevating the expressions of Keap-1. Additionally, PFOS exposure increased the activities of biochemical markers i.e., SOD, GPx, CAT, GST, GSH, GSR, and HO-1. Furthermore, remarkable increase was observed in the levels of malondialdehyde (MDA) and reactive oxygen species (ROS). Moreover, PFOS exposure elevated the levels of troponin I, creatine kinase-MB (CK-MB), lactate dehydrogenase (LDH), creatine phosphokinase (CPK), and inflammatory markers (COX-2, TNF-α, IL-1β, NF-κB, and IL-6). Besides, the expressions of Bcl-2 were downregulated and the expressions of Bax and Caspase-3 were upregulated after exposure to PFOS. Moreover, the normal architecture of the heart tissues was damaged after the administration of PFOS. However, supplementation of PLG protected the cardiac tissues from PFOS induced damage due to its remarkable anti-inflammatory, antioxidative and antiapoptotic characteristics.