Protective role of poncirin against polyethylene microplastics instigated cardiac toxicity via regulating Nrf2/keap1 pathway
Yasmeen Rasheed1, Nazia Ehsan1, Muhammad Faisal Hayat1, Asma Ashraf2, Hammad Ahmad Khan1, Aisha Khatoon3, Muhammad Umar Ijaz1*, Yasir S. Raouf4, Abdelouahid Samadi4*, Samir Chtita5
1Department of Zoology, Wildlife and Fisheries, University of Agriculture, Faisalabad 38040, Pakistan
2Department of Zoology, Government College University, Faisalabad 38000, Pakistan
3Department of Pathology, University of Agriculture, Faisalabad 38040, Pakistan
4Department of Chemistry, College of Science, United Arab Emirates University, Ai-Ain P.O. Box 15551, United Arab Emirates
5Laboratory of Analytical and Molecular Chemistry, Faculty of Sciences Ben M’Sik, Hassan II University of Casablanca, P.O. Box No. 7955, Casablanca, Morocco
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.
