CAJ | 학술논문

目的探讨拉科酰胺对神经病理性痛大鼠背根神经节(DRG)Nav1.8表达的影响.方法 SPF级雌性SD大鼠36只,体重120～130 g,采用随机数字表法,将其随机分为3组(n=12):假手术组(S组)、模型组(M组)、拉科酰胺组(L组).M组和L组将钢棒插入椎间孔压迫L5DRG制备神经病理性痛模型.于术前2 d、术后2,4、6、7、8、9、10 d(T0-7)时测定机械痛阈.于T4时,S组和L组腹腔注射拉科酰胺20 mg/kg(生理盐水溶解至0.5 ml),M组注射生理盐水0.5 ml,2次/d,连续4 d.每天末次给药后测定痛阈.于T7时痛阈测定后取术侧L5DRG,采用RT-PCR法和免疫组织化学法测定Nav1.8mRNA和蛋白表达水平.结果与S组比较,M组和L组T1～7时机械痛阚降低,Nav1.8 mRNA和蛋白表达上调(P<0.05);与M组比较,L组T4～7时机械痛阈升高,Nav1.8 mRNA和蛋白表达下调(P<0.05).结论拉科酰胺减轻大鼠慢性神经病理性痛的机制与下调损伤DRG的Nav1.8表达有关.
목적 탐토랍과선알대신경병이성통대서배근신경절(DRG)Nav1.8표체적영향.방법 SPF급자성SD대서36지,체중120～130 g,채용수궤수자표법,장기수궤분위3조(n=12):가수술조(S조)、모형조(M조)、랍과선알조(L조).M조화L조장강봉삽입추간공압박L5DRG제비신경병이성통모형.우술전2 d、술후2,4、6、7、8、9、10 d(T0-7)시측정궤계통역.우T4시,S조화L조복강주사랍과선알20 mg/kg(생리염수용해지0.5 ml),M조주사생리염수0.5 ml,2차/d,련속4 d.매천말차급약후측정통역.우T7시통역측정후취술측L5DRG,채용RT-PCR법화면역조직화학법측정Nav1.8mRNA화단백표체수평.결과 여S조비교,M조화L조T1～7시궤계통감강저,Nav1.8 mRNA화단백표체상조(P<0.05);여M조비교,L조T4～7시궤계통역승고,Nav1.8 mRNA화단백표체하조(P<0.05).결론 랍과선알감경대서만성신경병이성통적궤제여하조손상DRG적Nav1.8표체유관.
Objective To investigate the effect of lacosamide on expression of Nav1 .8 in dorsal root ganglia (DRG) in a rat model of chronic neuropathic pain.Methods Thirty-six female specific-pathogen-free (SPF)SD rats were randomly assigned into 3 groups ( n = 12 each): sham operation group (group S), model group (group M) and lacosamide group (group L) . Chronic neuropathic pain was produced by insertion of a small stainless steel rod (4.00 mm in length and 0.63 mm in diameter) into the L, intervertebral foramen in the rat, producing a chronic steady compression of the DRG in M and L groups. The mechanical threshold was measured 2 days before operation and on the 2, 4, 6, 7, 8, 9 and 10 days after operation (T0-7 ) . Intraperitoneal lacosamide 20mg/kg (in normal saline 0.5 ml) was injected at T4-7, twice a day in S and L groups. In group M, normal saline 0.5 ml was injected at T4-7 twice a day and the mechanical threshold was measured after the last administration everyday . The L, DRG on the operated side was removed after measurement of pain threshold to detect the expression of Na, 1.8 mRNA and protein by RT-PCR and immuno-histochemistry respectively. Results Compared with group S, the mechanical pain threshold was significantly decreased at T1-7 and the expression of Navl .8 mRNA and protein was up-regulated in M and L groups ( P < 0.05) . Compared with group M, the mechanical pain threshold was significantly increased at T4-7 and the expression of Nav 1.8 mRNA and protein was down-regulated in group L ( P < 0.05) . Conclusion The mechanism by which lacosamide reduces chronic neuropathic pain is related to the down-regulation of the expression of Nav 1.8 in rat DRG.