Potential effects of long-term nanoselenium administration on memory deficits associated with peripheral neuropathic pain through alteration of hippocampal Tau and proinflammatory cytokines.

Background: Chronic neuropathic pain is frequently associated with memory disorders linked to hippocampal alteration. Recognizing this co-morbidity could enhance treatment effectiveness. Prior studies have shown that nanoselenium possesses pain-relieving and memory-protecting properties, suggesting its potential in treating neuropathic pain and its associated co-morbidity.

Objective: This study aimed to examine the effects of long-term nanoselenium administration on pain-related behaviors and co-morbid memory disorders in rats with chronic constriction injury (CCI) of the sciatic nerve.

Methods: The study involved 32 adult male albino Wistar rats, divided into four groups: Control, CCI, CCI+nanoselenium, and CCI+vehicle (n = 8, each group). Nanoselenium or vehicle was administered intraperitoneally for two weeks after CCI surgery. Pain-related behavior was assessed using the acetone test and the Randal-Selitto test, while memory-related behavior was evaluated using a passive avoidance (shuttle-box) test. Additionally, the study involved identifying Tau positive cells through an Immunohistochemistry procedure and measuring IL-1 and TNF levels in the hippocampus using an enzyme-linked immunosorbent assay (ELISA) to explore potential relationships.

Results: The data indicated that CCI results in chronic neuropathic pain-related behaviors and memory disorders in rats. Long-term treatment with nanoselenium significantly increased pain threshold (F(1,3)=184.261, P = 0.000), improved memory (F(3,28)=170.726 ,F(3,28)=128.177,F(3,28)=41.552, P = 0.000) and decreased the hippocampal levels of IL-1β (F(3,28)=62.68, P = 0.000), TNFα (F(3,28)=173.12, P = 0.000), and the Tau positive cells/mm³ (F(3,28)=45.26, P = 0.000) in CA1 region in CCI rats.

Conclusion: Long-term administration of nanoselenium ameliorated pain-related behavior and improved memory disorder induced by CCI. This effect was associated with altered pro-inflammatory and Tau protein in the rats' hippocampus.