Role of transient receptor potential channel 8 in development and maintenance of neuropathic pain in rats: the relationship with nuclear factor kappa B in dorsal root ganglion / 中华麻醉学杂志

ABSTRACT

Objective To evaluate the role of transient receptor potential channel 8 (TRPM8) in the development and maintenance of neuropathic pain and the relationship with nuclear factor kappa B (NF-κB) in the dorsal root ganglion of rats.Methods Thirty-six pathogen-free healthy adult male SpragueDawley rats,weighing 180-200 g,aged 6-8 weeks,were divided into 3 groups (n=12 each) using a random number tablesham opeation group (group S),neuropathic pain group (group NP) and TRPM8 bocker BCTC group (group BCTC).Neuropathic pain was induced by ligation of the right sciatic nerve in anesthetized rats.BCTC 20 nmol was intrathecally injected once a day on preoperative day 1 and postoperative days 1,3,7 and 10 in group BCTC.The thermal,mechanical and cold pain thresholds were measured on preoperative day 1 and postoperative days 1,3,7,10 and 14.The dorsal root ganglions of the lumbar segment (L4-6) were removed on postoperative days 7 and 14 for determination of the expression of TRPM8 and NF-κB p65 by Western blot.Results Compared with group S,the thermal and mechanical thresholds were significantly decreased on postoperative days 1-14,and the cold pain threshold was decreased on postoperative days 3-14 in NP and BCTC groups,the expression of TRPM8 and NF-κB p65 in dorsal root ganglions was up-regulated on postoperative days 7 and 14 in group NP (P＜0.05),and no significant change was found in the expression of TRPM8 and NF-κB p65 in dorsal root ganglions in group BCTC (P＞0.05).Compared with group NP,the thermal pain threshold was significantly decreased and the cold pain threshold was increased on postoperative days 3-14,the expression of TRPM8 and NF-κB p65 in dorsal root ganglions was up-regulated on postoperative days 7 and 14,and no significant change was found in the mechanical pain threshold in group BCTC (P＞0.05).Conclusion NF-κB activation after opening of TR-PM8 in dorsal root ganglion neurons is involved in the development and maintenance of neuropathie pain in rats.