Abstract: Objective:?To explore the relationship between dental pulp fibroblast (DPF) lactate accumulation and inflammation in pulpitis. Methods:? SD rats were used to construct the pulpitis model. Hematoxylin-eosin was used to observe the inflammatory infiltration of pulpitis. The expression of inflammatory cytokines, IL-1β and TNF-α, as well as the key enzyme that catalyzes lactate production, lactate dehydrogenase A (LDHA), were visualized by immunohistochemical staining. Immunofluorescence staining was used to evaluate the colocalization of LDHA and the marker of dental pulp fibroblasts Vimentin. Human health and carious third molars were collected, then extracting normal and inflammatory pulp tissues to measure lactate content. DPF was cultured in vitro and LDHA inhibitor GSK2837808A was added. The cells were divided into control group, lipopolysaccharide (LPS) group, and LDHA inhibitor group. Lactate test kit was used to measure cellular lactate content. qRT-PCR was used to detect the mRNA expression of inflammatory cytokines IL-1β and TNF-α, and LDHA. Results:? Compared with the normal pulp of rats,the inflammatory infiltration increased during the modeling of pulpitis for 1d，3d, meanwhile the expression of LDHA and inflammatory cytokines IL-1β, TNF-α increased ,especially3d (P＜0.05),while decreased at 7 days, which has no significant difference as compared with that of the control group (P＞0.05). Vimentin and LDHAof DPF in inflammatory pulp tissue in rats could be seen co-localization. The content of lactate in human inflammatory pulp tissue was higher than that of healthy pulp (P＜0.05). By treating dental pulp fibroblasts with lactate dehydrogenase inhibitor GSK2837808A, lactate secretion decreased, and the expression of LDHA and inflammatory cytokines decreased (P＜0.05). Conclusions:?In the development of pulpitis, the production of lactate of DPF is related to the degree of inflammation, and the accumulation of lactate promoted the expression of inflammatory cytokines;and by inhibiting LDHA,human DPFlactate production and expression of inflammatory factors were reduced.

Key words: lactate, lactate dehydrogenase, pulpitis, dental pulp fibroblasts