Camphor Ameliorates Cadmium-induced Memory Deficits in Rats by Downregulating NF-κB and Enhancing Acetylcholine Signaling in the Hippocampus.

Cadmium (Cd) is a toxic heavy metal that can penetrate the blood-brain barrier, leading to harmful effects on the nervous system by disrupting the brain's antioxidant defense mechanisms. This research investigates how camphor, a natural compound recognized for its antioxidant effects, influences biochemical, molecular, and histological alterations in the hippocampus of rats exposed to cadmium. It also assesses its influence on the spatial memory abilities of these animals. Adult male Wistar rats were divided into four groups, each containing 10 rats: Control, Camphor, Cd, and Cd + Camphor. Cadmium chloride (5 mg/kg, orally) and camphor (10 mg/kg, intraperitoneally) were administered for 21 consecutive days. The findings revealed that treatment with camphor resulted in elevated levels of GSH, improved activities of SOD and GPx, and reduced MDA levels in the hippocampus of rats exposed to cadmium chloride. Moreover, camphor decreased the expression of pro-inflammatory cytokines, such as TNF-α, IL-1β, and IL-6, while increasing the expression of IL-10. In addition, camphor diminished mRNA and protein amounts of NF-κB in the hippocampus and reduced neuronal death in the CA1 area. It decreased the expression and activity of acetylcholinesterase, enhanced the expression of BDNF and the alpha-7 nicotinic acetylcholine receptor in the hippocampus, and caused a significant improvement in spatial memory. We conclude that camphor enhanced spatial memory in rats exposed to cadmium chloride by alleviating oxidative stress, reducing neuroinflammation, and preventing neuronal loss. It plays a vital role in protecting the hippocampus by lowering NF-κB expression and boosting acetylcholine signaling.