The Mitigation of Quercetin on Lead-induced Neuroinflammation in a Rat Model: Changes in Neuroinflammatory Markers, Hippocampal Neurons and Memory

The present study investigated the mitigatory effects of quercetin on neuroinflammation, hippocampal degeneration, and memory deficits in lead (Pb)-exposed rats. Wistar rats were administered orally with quercetin and succimer (standard drug) for 21 days after Pb exposure of 21 days or in combination with Pb for 42 days. Working and reference memory was assessed using an eight-arm radial water maze (8-ARWM). The changes in brain Pb level, the neuronal nitric oxide synthase (nNOS) activity, and the level of neuroinflammatory markers like tumour necrosis factor-alpha (TNF-α) and interleukin 1 Beta (IL-1β) were determined. The number of neurons and astrocyte expression were all evaluated histologically and immunohistochemically, respectively. The brain level of Pb was increased significantly in Pb-exposed rats. In the hippocampus, the number of neurons decreased while the expression of astrocytes increased, and the levels of neuroinflammatory markers increased in Pb-exposed rats. Lead impaired reference and working memory. However, quercetin treatment effectively reduced neuronal loss, improved memory, and inhibited neuroinflammation. In conclusion, quercetin mitigates neuroinflammation, hippocampal degeneration, and memory deficits in Pb-exposed rats. Neuroinflammatory markers negatively correlated with memory function. Thus, quercetin may be a promising therapy in neuroinflammation and memory dysfunction in populations prone to Pb exposure.