Neuroprotective Effects of Myricitrin on Cognitive Deficits in Hippacampal Demyelinated Rats

Background and purpose: Multiple sclerosis (MS) as an autoimmune disease is the most common demyelinating inflammatory disease in young people that affects the central nervous system. Myricitrin (MYR) is known to have antioxidant and neuroprotection effects, so, the current study investigated its effect on cognitive defects in rat models of MS. Materials and methods: In this experimental study, 40 Wistar rats were divided into five groups. Intra- hippocampus injection of Ethidium bromide (3 µL 0.01%) was performed using Hamilton syringe to induce demyelination. MYR was injected intraperitoneally for seven days after induction of demyelination. Measurements of passive avoidance memory in shuttle box, spatial memory (using Morris water maze), balance (by rotarod task), and anxiety level (using elevated plus maze) were done. The levels of MDA, TNF-α, and total antioxidant capacity were also measured. Results: Ethidium bromide significantly increased hippocampal MDA and TNF-α levels and decreased hippocampal total antioxidant capacity activity (P< 0.001). MYR treatment significantly prevented the decrease of antioxidant capacity and the increase in hippocampal MDA and TNF-α levels induced by ethidium bromide (P< 0.05 and P< 0.001, respectively). Behavioral evaluation also indicated that treatment with MYR significantly improved the ability to keep information and reminders, spatial memory, balance, and anxiety. Conclusion: Injection of ethidium bromide into the CA1 region of the hippocampus led to the induction of MS, and administration of MYR may improve memory, motor function, and anxiety in MS models, possibly through antioxidant and anti-inflammatory pathways.