CAJ | 학술논문

目的评价丹参酮ⅡA磺酸钠对神经病理性痛大鼠脊髓人CX3C趋化因子受体1(CX3CR1)、NF-κB及TN'F-α mRNA表达的影响.方法雄性Wistar大鼠54只,体重180 ～ 220 g,6～8周龄,采用随机数字表法,将大鼠分为3组:假手术组(S组)、神经病理性痛组(CCI组)和丹参酮ⅡA磺酸钠组(SSI组),每组18只.CCI组和SSI组采用坐骨神经慢性压迫损伤法制备大鼠神经病理性痛模型.SSI组于术毕即刻开始至处死前1d,腹腔注射丹参酮ⅡA磺酸钠注射液25 mg/kg,1次/d,S组和CCI组腹腔注射等容量(5 ml/kg)生理盐水.于术前1d、术后3、7和14 d(T0-3时测定机械痛阈和热痛阈;于T1-3时测定痛阈后处死大鼠,取L4-6脊髓组织,采用荧光定量PCR法测定脊髓CX3CR1、NF-κB及TNF-α的mRNA表达.结果与S组比较,CCI组和SSI组术后T1-3时机械痛阈和热痛阈降低,脊髓CX3CR1、NF-κB及TNF-α的mRNA表达上调(P＜0.05);与CCI组比较,SSI组术后T1-3时机械痛阈和热痛阈升高,脊髓CX3CR1、NF-κB及TNF-α的mRNA表达下调(P＜0.05).与L时比较,CCI组、SSI组于T2和T3时CX3CR1表达下调,NF-κB和TNF-α的mRNA表达上调(P＜0.05);与T2时比较,CCI组、SSI组T3时CX3CR1、NF-κB和TNF-α的mRNA表达下调(P＜0.05).结论丹参酮ⅡA磺酸钠减轻大鼠神经病理性痛的机制与抑制NF-κB的激活,下调CX3CR1及TNF-α mRNA的表达有关.
목적 평개단삼동ⅡA광산납대신경병이성통대서척수인CX3C추화인자수체1(CX3CR1)、NF-κB급TN'F-α mRNA표체적영향.방법 웅성Wistar대서54지,체중180 ～ 220 g,6～8주령,채용수궤수자표법,장대서분위3조:가수술조(S조)、신경병이성통조(CCI조)화단삼동ⅡA광산납조(SSI조),매조18지.CCI조화SSI조채용좌골신경만성압박손상법제비대서신경병이성통모형.SSI조우술필즉각개시지처사전1d,복강주사단삼동ⅡA광산납주사액25 mg/kg,1차/d,S조화CCI조복강주사등용량(5 ml/kg)생리염수.우술전1d、술후3、7화14 d(T0-3시측정궤계통역화열통역;우T1-3시측정통역후처사대서,취L4-6척수조직,채용형광정량PCR법측정척수CX3CR1、NF-κB급TNF-α적mRNA표체.결과 여S조비교,CCI조화SSI조술후T1-3시궤계통역화열통역강저,척수CX3CR1、NF-κB급TNF-α적mRNA표체상조(P＜0.05);여CCI조비교,SSI조술후T1-3시궤계통역화열통역승고,척수CX3CR1、NF-κB급TNF-α적mRNA표체하조(P＜0.05).여L시비교,CCI조、SSI조우T2화T3시CX3CR1표체하조,NF-κB화TNF-α적mRNA표체상조(P＜0.05);여T2시비교,CCI조、SSI조T3시CX3CR1、NF-κB화TNF-α적mRNA표체하조(P＜0.05).결론 단삼동ⅡA광산납감경대서신경병이성통적궤제여억제NF-κB적격활,하조CX3CR1급TNF-α mRNA적표체유관.
Objective To evaluate the effects of Tanshinone Ⅱ A Sulfotanshinone Sodium Injection (SSI) on the expression of CX3C chemokine receptor 1 (CX3CR1),nuclear factor kappa B (NF-gB) and tumor necrosis factor-α (TNF-α) mRNA in a rat model of neuropathic pain.Methods Fifty-four male Wistar rats,weighing 180-220 g,aged 6-8 weeks,were randomly assigned into 3 groups (n =18 each) using a random number table:sham operation group (group S),chronic constrictive injury (CCI) group,and group SSI.In group S,the right sciatic nerves were exposed but not ligated,and in CCI and SSI groups,4 ligatures were placed around the right sciatic nerve according to Bennett's method.In group SSI,SSI 25 mg/kg was injected intraperitoneally once a day starting from the end of operation until one day before the animals·were sacrificed,while the rats received the equal volume of normal saline (5 ml/kg) instead of SSI in S and CCI groups.Mechanical withdrawal threshold (MWT) and thermal withdrawal latency (TWL) were measured on the day before CC1 and 3rd,7th and 14th days after CCI (T0-3).Six animals were randomly sacrificed after measurement of pain threshold on 3rd,7th and 14th days after CCI in each group,and the L4-6 segments of spinal cords were removed for determination of CX3CR1,NF-κB and TNF-α mRNA expression by real-time fluorescent quantitative PCR.Results Compared with group S,MWT and TWL were significantly decreased,and the expression of CX3CR1,NF-κB and TNF-α mRNA was up-regulated at T1-3 in CCI and SSI groups.Compared with group CCI,TWL and MWT were significantly increased,and the expression of CX3CR1,NF-κB and TNF-α mRNA was down-regulated at T1-3 in group SSI.The expression of CX3CR1 mRNA was down-regulated,and the expression of NF-κB and TNF-α mRNA was higher at T2.3 than at T1 in CCI and SSI groups.The expression of CX3CR1,NF-κB and TNF-α mRNA was lower at T3 than at T2 in CCI and SSI groups.Conclusion The mechanism by which Tanshinone Ⅱ A SSI attenuates neuropathic pain is related to inhibition of NF-κB activation and down-regulation of CX3CR1 and TNF-α mRNA expression in rats.