OBJECTIVETo investigate the relationship between pulpitis pain and voltage-gated sodium channel (Nav1.9) by detecting the expression of Nav1.9 at different time points of the rat pulpal lesion model.

METHODSThirty-six SD pulpal lesions rat models were divided into three experimental groups, 1 d (n = 12), 3 d (n = 12) and 5 d group(n = 12).Normal SD rats served as control(n = 12). Tumor necrosis factor-α (TNF-α) and Nav1.9 mRNA expressions were evaluated by reverse transcription PCR (RT-PCR) .Nav1.9 protein expressions were analyzed by enzyme-linked immunosorbent assay (ELISA) and Western blotting.

RESULTSThe expression of TNF-α in the experimental group (1 d:0.514 ± 0.098, 3 d:0.739 ± 0.104, 5 d:1.238 ± 0.082) was higher than those in the control group (0.147 ± 0.016) (P < 0.01). Nav1.9 mRNA was up-regulated markedly in experimental groups (1 d: 0.296 ± 0.038, 3 d:0.409 ± 0.013, 5 d: 0.487 ± 0.028) , compare with control group (0.223 ± 0.020) (P < 0.05). The ELISA results revealed that the level of Nav1.9 in control pulp tissue was (4.013 ± 0.292) µg/L, in painful pulp tissue of 1 d group was (5.143 ± 0.101) µg/L, in painful pulp tissue of 3 d group was (5.835 ± 0.088) µg/L and in painful pulp tissue of 5 d group was (6.307 ± 0.137) µg/L (P < 0.05). Western blotting showed the expression of Nav1.9 in experimental groups (1 d: 0.106 ± 0.007, 3 d:0.170 ± 0.013, 5 d:0.238 ± 0.004) was up-regulated significantly compared with control group (0.073 ± 0.004)(P < 0.05).

CONCLUSIONSThe level of Nav1.9 had a significant increase in painful pulp tissue. Moreover, with the degree of pain aggravation, the expression of Nav1.9 increased in pulp tissue.It suggests that Nav1.9 may play an important role in the development of pulpitis pain.