The Potential Protective Effects of Quercetin Treatment onHippocampal Tissue of Wistar Rats Exposed to Cadmium

This study aimed to assess the neuroprotective potential of quercetin (Q) againstcadmium (Cd)-induced toxicity by evaluating its impact on antioxidant enzymeactivities, cytokine profiles, neuronal survival, and histopathological alterationsin the hippocampal tissue of rats. Twenty four healthy male Wistar albino ratswere randomly assigned into four groups: control (C; n = 6), cadmium (Cd; n= 6), quercetin (Q; n = 6), and cadmium + quercetin (Cd+Q; n = 6). CdCl₂ wasadministered subcutaneously at 4 mg/kg/day for three days to the Cd and Cd+Qgroups. Simultaneously, quercetin was administered intraperitoneally at 50 mg/kg/day to the Q and Cd+Q groups. The hippocampal tissues were collected post-treatment for biochemical, histopathological, and cellular analyses. Cadmiumexposure led to oxidative stress, elevated pro-inflammatory cytokines, suppressedantioxidant defenses, and neuronal degeneration in the hippocampus. Quercetintreatment partially mitigated these effects by enhancing antioxidant markers (GSH,SOD), modulating cytokine levels (notably IL-1), and preserving neuronal integrity,particularly in the CA1, CA2, CA3, and dentate gyrus regions (p < 0.05). Thesefindings suggest that quercetin confers partial neuroprotection against cadmium-induced hippocampal damage through its antioxidative and anti-inflammatoryproperties. While not entirely preventive, quercetin may serve as a supportivetherapeutic agent in countering heavy metal-induced neurotoxicity.