Changes in expression of Ac-H3 and SIRT1 in dorsal root ganglions in a rat model of negative phenotype neuropathic pain
10.3760/cma.j.issn.0254-1416.2014.01.009
- VernacularTitle:阴性表型神经病理性痛大鼠背根神经节Ac-H3和SIRT1表达的变化
- Author:
Xin HE
;
Changsheng HUANG
;
Yu ZOU
;
Xiang LI
;
Qulian GUO
- Publication Type:Journal Article
- Keywords:
Neuralgia;
Histones;
Acetylation;
Sirtuins;
Ganglia,spinal
- From:
Chinese Journal of Anesthesiology
2014;34(1):33-36
- CountryChina
- Language:Chinese
-
Abstract:
Objective To evaluate the changes in the expression of acetylated histone H3 (Ac-H3) and deacetylase silent information regulator 1 (SIRT1) in dorsal root ganglions in a rat model of negative phenotype neuropathic pain.Methods Forty-eight male Sprague-Dawley rats,weighing 250-300 g,were randomly divided into 2 groups (n =24 each):sham operation group (group S) and C-fiber dysfunction group (group CFD).The rats were anesthetized with 10% chloral hydrate 3 ml/kg.C-fiber dysfunction was induced by exposing sciatic nerve to 8% capsaicin for 30 min in group CFD.The thermal withdrawal latency (TWL) and mechanical withdrawal threshold (MWT) were measured before and on 1,3,7 and 14 days after CFD.Six rats were then sacrificed at each time and the lumbar segments (L5) of the dorsal root ganglions were removed for detection of SIRT1 mRNA expression (by RT-PCR) and Ac-H3 and SIRT1 protein expression (by Western blot).Results Compared with group S,TWL was significantly increased at 1,3,7 and 14 days after CFD,SIRT1 mRNA and protein expression was up-regulated and Ac-H3 expression was down-regulated at 3,7 and 14 days after CFD (P < 0.05),while no significant change was found in MWT at each time point in group CFD (P > 0.05).Conclusion The mechanism of negative phenotype neuropathic pain is related to up-regulation of deacetylase SIRT1 expression and decreased acetylation of histone H3 in rat dorsal root ganglions.