2024 Volume 39 Issue 1 Pages 46-52
Fatty acid–binding protein 3 (FABP3) is involved in intracellular lipid transport to cytosolic organelles. It also performs unique physiological functions, acting as a diagnostic or predictive biomarker for various diseases. We previously reported that hypothalamic FABP3 levels are upregulated under pain and that FABP3 is co–expressed in microglia. However, the specific roles of FABP3 in microglia remain unknown. Therefore, in this study, we aimed to assess the involvement of FABP3 in lipopolysaccharide (LPS)–induced increase in inflammatory cytokine levels and determine its effects on pain in mouse microglial MG6 cells and postoperative pain model mice. MG6 cells were treated with LPS to activate the cells and the cytoplasmic fraction was collected as a sample after 24 hours. FABP–IN–1 was used as a non–selective FABP inhibitor, and FABP3 small interfering RNA (siFABP3) was used for FABP3 knockdown. Changes in the expression of each gene were analyzed via real–time polymerase chain reaction. In MG6 cells, LPS (100 and 1000 ng/mL) significantly increased the tumor necrosis factor–α, interleukin–6, and FABP3 mRNA levels; however, FABP–IN–1 or siFABP3 significantly suppressed this effect. Furthermore, repeated intracerebroventricular injection of FABP–IN–1 suppressed pain behavior in the postoperative pain model mice. Overall, our results suggest that FABP3 is partly involved in the induction of inflammatory cytokine expression via microglial activation, thereby affecting the pain behavior in brain.
