Abstract
Brain inflammation and oxidative stress play a critical role in the neuronal apoptosis and memory dysfunction in Alzheimer’s disease. Crocin is a natural carotenoid present in the stigma of saffron which possesses radical scavenging, anti-inflammatory, and anti-apoptotic properties. The present study examined the protective impact of crocin on neuronal apoptosis, oxidative stress, neuroinflammation and memory deficits induced by lipopolysaccharide (LPS) in rats. Wistar rats received crocin at a dose of 100 mg/kg for 12 days. Besides, LPS (1 mg/kg, ip) was injected on days 8–12. Spatial memory was evaluated in the Morris water maze, two hours after LPS injection on days 8–12. Gene expression of nuclear factor (NF)-κB, tumor necrosis factor-α (TNF-α), caspase 3 and lipid peroxidation was assessed in the hippocampal homogenates at the end of behavioral test. Histopathological changes in the hippocampus and cerebral cortex was evaluated using H&E staining. According to results, administration of LPS caused spatial memory dysfunction accompanied by upregulation of mRNA expression of NF-κB, TNF-α and caspase 3 as well as increased lipid peroxidation and tissue damge in the hippocampus. Furthermore, crocin treatment at a dose of 100 mg/kg attenuated memory impairments, downregulated the mRNA expression of NF-κB, TNF-α and caspase 3 and decreased lipid peroxidation in the hippocampus. Crocin also ameliorated LPS-induced pathological changes and neuronal loss in the hippocampus and cerebral cortex. In conclusion, neuroprotective effects of crocin against LPS-induced histopathological and behavioural changes could be attributed to its anti-apoptotic, anti-inflammatory and radical-scavenging activities in the rat brain.