Protective role of poncirin against polyethylene microplastics instigated cardiac toxicity via regulating Nrf2/keap1 pathway

Abstract

Polyethylene microplastics (PEMPs) are one of the most toxic pollutants in our surroundings that induce damage to various organs including heart. Poncirin (PON) is a natural flavonoid that shows diverse pharmacological activities. This study was aimed to assess the alleviative potential of PON against PEMPs provoked cardiac damage in rats. Twenty-four rats were segregated into 4 groups including control, PEMPs (1.5 mg/kg) treated group, PEMPs (1.5 mg/kg) + PON (5mg/kg) exposed group and PON (5mg/kg) alone treated group. It was revealed that PEMPs exposure notably decreased the expression of Nrf2 and its associated antioxidant genes while upregulating the expression of Keap-1. Besides, PEMPs intoxication reduced the activities of superoxide dismutase (SOD), catalase (CAT), heme-oxygenase-1 (HO-1), peroxidase (GPx), glutathione reductase (GSR), and glutathione (GSH) content while increasing reactive oxygen species (ROS) and malondialdehyde (MDA) levels. Additionally, exposure to PEMPs resulted in upregulation of lactate dehydrogenase (LDH), creatine kinase MB (CK-MB), troponin I and phosphokinase (CPK).  Besides, PEMPs administration escalated the levels of TNF- α IL-6, NF-κB, TNF- α, IL-1β, and COX-2 activity. Moreover, the administration of PEMPs escalated the levels of Caspase-3 and Bax, while downregulating the levels of Bcl-2. Additionally, PEMPs exposure disrupted the architecture of cardiac tissues. Nonetheless, PON supplementation remarkably protected the cardiac tissues by regulating the aforementioned damages.