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.