Objective: To explore the expression and significance of β-1,4-galactosyltransferase-I (β-1,4-GalT-I) and tumor necrosis factor-α (TNF-α) in dorsal root ganglia (DRG) of rat lumbar facet arthritis (LFA) model. Methods: Adult SD rats were randomly divided into control group and experimental group. For the experimental group, Freund′s complete adjuvant was used to make rat LFA model. Mechanical withdrawal threshold was used to test the change of the mechanical thresholds of the rat foot. The expression of β-1,4-GalT-I and TNF-α in rat DRG and the activation of mitogen activated protein kinase (MAPK) signaling pathway were detected by Western blotting. The distribution and co-localization of β-1,4-GalT-I and TNF-α in DRG of rats were detected by immunofluorescence double labeling. Results: Compared with the control group, the mechanical thresholds of the foot of rats in the experimental group on the 3rd, 5th and 7th days were significantly lower; β-1,4-GalT-I and TNF-α protein levels increased on the 3rd, 5th and 7th days and reached a peak on the 5rd day, and then gradually returned to normal levels in DRG; β-1,4-GalT-I and TNF-α were expressed in DRG neurons and glial cells, and the expression of β-1,4-GalT-I and TNF-α in the 5rd day DRG neurons and glial cells in the experimental group was significantly higher than that in the control group; There was colocalization between β-1,4-GalT-I and TNF-α and MAPK signaling pathways were also activated in DRG of the experimental group. Conclusion: Inflammation of LFA in rats can lead to increased expression of β-1,4-GalT-I and TNF-α in DRG neurons and glial cells, which may be closely associated with the neurological symptoms of lower limbs caused by LFA.

［Key words］lumbar facet arthritis; dorsal root ganglia; β-1,4-galactosyltransferase-I; tumor necrosis factor-α; inflammation