Expression Of Voltage Gated Sodium Channel Na_v1.9in Experimental Pulpal Lesions In The Rats

Objective Voltage gated sodium channel Nav1.9expressed specifically in primarysensory neurons, and played a critical role in the action potential current regulation.Nav1.9underlies pain linked to pathological injury and inflammation. The nerve fibersinitiated by the trigeminal ganglion in the pulp is nociceptor. To determine the degree ofpulpitis pain by observing behavior of rats, analyzing biopsy and detecting theexpression of tumor necrosis factor-α(TNF-α).The study investigated the relationshipbetween pulpitis pain and voltage-gated sodium channel （Nav1.9） by detecting theexpression of Nav1.9at different time points of the rat pulpal lesion model.Methods Thirty-Six SD pulpal lesions rat models were divided into three experimentalgroups,1d (n=12),3d (n=12) and5d group (n=12). Normal SD rats served as control(n=12). The expressions of TNF-α and Nav1.9mRNA were evaluated by reversetranscription PCR (RT-PCR). The expressions of Nav1.9protein were analyzed byenzyme linked immunosorbent assay (ELISA) and Western blotting.Results The expression of TNF-α in the experimental group (1d:0.514±0.098,3d:0.739±0.104,5d:1.238±0.082) was higher than those in the control group(0.147±0.016)(P<0.05). In addition, Nav1.9mRNA was up-regulated markedly inexperimental groups (1d:0.296±0.038,3d:0.409±0.013,5d:0.487±0.028), comparewith control(0.223±0.020)(P<0.05). The results of ELISA revealed that the level ofNav1.9in control pulp tissue was (4.013±0.292) μg/L, in painful pulp tissue of1d groupwas (5.143±0.101)μg/L, in painful pulp tissue of3d group was (5.835±0.088)μg/L and in painful pulp tissue of5d group was (6.307±0.137)μg/L,(P<0.05). Moreover, Westernblotting showed the expression of Nav1.9in experimental groups (1d:0.106±0.007,3d:0.170±0.013,5d:0.238±0.004) was up-regulated significantly compared with controlgroup (0.073±0.004),(P<0.05).Conclusions The results showed that the level of Nav1.9had a significant increase inpainful pulp tissue. Moreover, with the degree of pain aggravation, the expression ofNav1.9increased in pulp tissue. It indicated that Nav1.9may act as an important part tothe development of pulpitis pain. Moreover, specifically blocking the expression ofNav1.9or inhibiting the function of Nav1.9may impede inflammatory pain occurrence,resulting in a better analgesic effect. Nav1.9may be the new target of analgesic drugwith low side effects.