Background: Activation of microglia participates in a wide range of pathophysiological processes in the central nervous system. Some studies reported that oxycodone (6-deoxy-7,8-dehydro-14-hydroxy-3-O-methyl-6oxomorphine) could inhibit the overactivation of glial cells in rats’ spinal cords. In the present study, we observed the effect of oxycodone on inflammatory molecules and pathway in lipopolysaccharide (LPS)-stimulated primary microglia in rats.
Materials and methods: Neonatal rats’ primary microglia were exposed to various concentrations (25, 50, 100 ng/mL) of oxycodone for 1 h after LPS stimulation for 24 h. The levels of pro-inflammatory mediators, IL-1β, TNF-α, and TGF-β1/smad2/3 signaling pathway were measured. The activation situation of microglia and the expression of TβR1 were observed by immunofluorescence.
Results: Oxycodone at 25 ng/mL did not change the levels of proinflammatory molecules and TGF-β1/smad2/3 signaling pathway in primary microglia, which was increased by LPS. Oxycodone at 50 and 100 ng/mL could significantly suppress LPS-induced production of TNF-α and IL-1β and the expression of TNF-αmRNA, IL-1βmRNA, and TGF-β1/smad2/3 signaling pathway.
Conclusion: These findings indicate that oxycodone, at relatively high clinically relevant concentration, can inhibit inflammatory response in LPS-induced primary microglia. The detailed mechanism needs to be investigated in future.
Keywords: oxycodone, inflammatory, microglia