This study aimed to assess the neuroprotective potential of quercetin (Q) against cadmium (Cd)-induced toxicity by evaluating its impact on antioxidant enzyme activities, cytokine profiles, neuronal survival, and histopathological alterations in the hippocampal tissue of rats. Twenty four healthy male Wistar albino rats were 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 was administered subcutaneously at 4 mg/kg/day for three days to the Cd and Cd+Q groups. 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. Cadmium exposure led to oxidative stress, elevated pro-inflammatory cytokines, suppressed antioxidant defenses, and neuronal degeneration in the hippocampus. Quercetin treatment 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). These findings suggest that quercetin confers partial neuroprotection against cadmium-induced hippocampal damage through its antioxidative and anti-inflammatory properties. While not entirely preventive, quercetin may serve as a supportive therapeutic agent in countering heavy metal-induced neurotoxicity.