Role Of ?-1,3-Galactosyltransferase 2 In LPS-induced Rat Dental Pulp Inflammation

ObjectiveGlycosyltransferases are enzymes that catalyze the formation of a variety of glycoconjugates.Recent studies have demonstrated that glycoconjugates synthesized by specific glycosyltransferases play an important role in the nervous system.However,the role of ?-1,3-galactosyltransferase in the inflammation of the nervous system is unknown.Dental pulp inflammation may cause neurophysiological alterations in the trigeminal ganglion,and serve as a good model for investigating the inflammation and pain of the peripheral nervous system.In the present study,we investigated the role of ?-1,3-galactosyltransferase 2(b3galt2)in neuroinflammation using the dental pulp inflammatory model induced by LPS in rat.MethodsThe gene and protein expression levels of b3galt2 were determined by reverse transcription PCR and western blot analysis,respectively,and ELISA assays were used to measure the levels of LPS-associated cytokines in the trigeminal ganglion.TLR4/NF?B signaling pathway was evaluated by immunohistochemistry.ResultsOur results demonstrated that LPS-associated dental pulp inflammation activated neurons and satellite cells and up-regulated b3galt2 expression in the trigeminal ganglion.B3galt2 knockdown reduced the secretion of TNF? and IL-6 in the trigeminal ganglion.The expression of TLR4 and NF?B in the trigeminal ganglion were activated during inflammation,but b3galt2 knockdown inhibited the expression of TLR4 and NF?B.ConclusionsThese observations indicated that inflammation could induce b3galt2 expression,and that b3galt2 might exert a protective role in dental pulp inflammation.Our results also suggested that b3galt2 may play an important role in mediating peripheral neuroinflammation via TLR4/ NF?B signaling pathway.