EFFECT OF POST-WEANING BISPHENOL A EXPOSURE ON COGNITION AND INFLAMMATORY MARKERS IN THE HIPPOCAMPUS: POSSIBLE ROLE OF SILYMARIN

Bisphenol A is a chemical compound primarily used in the manufacturing of polycarbonate plastics and epoxy resins. It is an example of an enivironmental toxicant. BPA is known as an endocrine distruptor especially in inflammatory pathways. This study aimed to investigate the influence of post-weaning bisphenol A on inflammatory markers, neurotransmitter levels, and hippocampus histopathology in male Wistar rats, and also the potential protective effects of silymarin, known as an antioxidant. Thirty-two newly weaned male Wistar rats were randomized into four groups; a control group, bisphenol A-treated group, silymarin-treated group, and bisphenol A + silymarin-treated group. Animals were administered daily for eight weeks via oral gavage. The BPA-treated group received 100mg/kg of BPA, while the silymarin group were administered 50mg/kg of silymarin. Blood and hippocampus samples were collected at the end of the study, and biochemical assays were performed to measure inflammatory markers, including dopamine, acetylcholinesterase, interleukin-1beta (IL-1B), myeloperoxidase (MPO), serotonin, tumor necrosis factors-a (TNF-a) and noradrenaline. Histological analysis of the hippocampal tissues was also conducted. The result shows that exposure to BPA drastically increased inflammation, by increasing TNF-α, IL-1β, MPO, decreased dopamine, increased acetylcholinesterase, decreased serotonin, and decreased noraderanalin. Neurotransmitter disruptors, including decreased dopamine, noradrenaline and serotonin, were observed in the BPA-treated groups, suggesting neurotoxicity. Histopathological evaluation revealed disrupted hippocampal screening in BPA-treated rats, with focal inflammatory cell filtration. However, silymarin administration lessen these biochemical and histological changes, revealing its protective impact against BPA-induced neurotoxicity.