中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2012年
3期
353-357
,共5页
王一涵%冷玉芳%李娟%韩雪娜
王一涵%冷玉芳%李娟%韓雪娜
왕일함%랭옥방%리연%한설나
右美托咪啶%细胞凋亡%后角细胞%神经痛
右美託咪啶%細胞凋亡%後角細胞%神經痛
우미탁미정%세포조망%후각세포%신경통
Dexmedetomidine%Apoptosis%Posterior horn cells%Neuralgia
目的 评价右美托咪啶对神经病理性痛大鼠脊髓背角神经元凋亡的影响.方法 健康成年雄性SD大鼠72只,体重180~220 g,采用随机数字表法,将其随机分为3组(n=24):假手术组(S组)、慢性神经病理性痛组(CNP组)和右美托咪啶组(D组).S组仅分离坐骨神经但不结扎,CNP组和D组采用结扎坐骨神经的方法制备大鼠神经病理性痛模型,D组于结扎坐骨神经结束开始至处死前,腹腔注射右美托咪啶50μg/kg,1次/d,S组和CNP组注射等容量生理盐水.于术前1d、术后3、7、14 d(T0-3)时测定大鼠机械缩足阈值(MWT)和热缩爪潜伏期(TWL);于T1-3时测定痛阈后每组随机处死8只大鼠,取L4,5脊髓组织,采用免疫组化法检测脊髓背角Bcl-2及caspase-3的表达水平,采用透射电镜观察脊髓背角浅层神经元超微结构.结果 与S组比较,CNP组和D组T1-3时MWT降低,TWL缩短,脊髓背角Bcl-2和caspase-3表达上调(P<0.05);与CNP组比较,D组T1 -3时MWT升高,TWL延长,脊髓背角Bcl-2表达上调,caspase-3表达下调(P<0.05).脊髓背角浅层神经元超微结构:S组基本正常,CNP组细胞凋亡数目增加,D组细胞凋亡数目较CNP组减少.结论 腹腔注射右美托咪啶可减轻大鼠慢性神经病理性痛,其机制可能与抑制脊髓背角神经元凋亡有关.
目的 評價右美託咪啶對神經病理性痛大鼠脊髓揹角神經元凋亡的影響.方法 健康成年雄性SD大鼠72隻,體重180~220 g,採用隨機數字錶法,將其隨機分為3組(n=24):假手術組(S組)、慢性神經病理性痛組(CNP組)和右美託咪啶組(D組).S組僅分離坐骨神經但不結扎,CNP組和D組採用結扎坐骨神經的方法製備大鼠神經病理性痛模型,D組于結扎坐骨神經結束開始至處死前,腹腔註射右美託咪啶50μg/kg,1次/d,S組和CNP組註射等容量生理鹽水.于術前1d、術後3、7、14 d(T0-3)時測定大鼠機械縮足閾值(MWT)和熱縮爪潛伏期(TWL);于T1-3時測定痛閾後每組隨機處死8隻大鼠,取L4,5脊髓組織,採用免疫組化法檢測脊髓揹角Bcl-2及caspase-3的錶達水平,採用透射電鏡觀察脊髓揹角淺層神經元超微結構.結果 與S組比較,CNP組和D組T1-3時MWT降低,TWL縮短,脊髓揹角Bcl-2和caspase-3錶達上調(P<0.05);與CNP組比較,D組T1 -3時MWT升高,TWL延長,脊髓揹角Bcl-2錶達上調,caspase-3錶達下調(P<0.05).脊髓揹角淺層神經元超微結構:S組基本正常,CNP組細胞凋亡數目增加,D組細胞凋亡數目較CNP組減少.結論 腹腔註射右美託咪啶可減輕大鼠慢性神經病理性痛,其機製可能與抑製脊髓揹角神經元凋亡有關.
목적 평개우미탁미정대신경병이성통대서척수배각신경원조망적영향.방법 건강성년웅성SD대서72지,체중180~220 g,채용수궤수자표법,장기수궤분위3조(n=24):가수술조(S조)、만성신경병이성통조(CNP조)화우미탁미정조(D조).S조부분리좌골신경단불결찰,CNP조화D조채용결찰좌골신경적방법제비대서신경병이성통모형,D조우결찰좌골신경결속개시지처사전,복강주사우미탁미정50μg/kg,1차/d,S조화CNP조주사등용량생리염수.우술전1d、술후3、7、14 d(T0-3)시측정대서궤계축족역치(MWT)화열축조잠복기(TWL);우T1-3시측정통역후매조수궤처사8지대서,취L4,5척수조직,채용면역조화법검측척수배각Bcl-2급caspase-3적표체수평,채용투사전경관찰척수배각천층신경원초미결구.결과 여S조비교,CNP조화D조T1-3시MWT강저,TWL축단,척수배각Bcl-2화caspase-3표체상조(P<0.05);여CNP조비교,D조T1 -3시MWT승고,TWL연장,척수배각Bcl-2표체상조,caspase-3표체하조(P<0.05).척수배각천층신경원초미결구:S조기본정상,CNP조세포조망수목증가,D조세포조망수목교CNP조감소.결론 복강주사우미탁미정가감경대서만성신경병이성통,기궤제가능여억제척수배각신경원조망유관.
Objective To investigate the effects of dexmedetomidine (Dex) on the neuronal apoptosis in spinal dorsal horn in a rat model of chronic neuropathic pain.Methods Seventy-two adult male SD rats weighing 180-220 g were randomly divided into 3 groups ( n =24 each):sham operation group (group S) ; chronic constrictive injury (CCI) group; Dex + CCI group (group D).Two ligatures were placed on right sciatic nerve at 1 mm intervals with 4-0 silk thread in groups CCI and D.In group D Dex 50 μg/kg was injected intraperitoneally once a day starting from the end of operation until the animals were sacrificed.Paw withdrawal threshold to mechanical stimulation with yon Frey filament (PWT) and paw withdrawal latency to thermal stimulation (PWL) were measured at one day before (T0,baseline) and on the 3rd,7th and 14th day after operation (T1,2,3).Six animals were sacrificed at each time points (T1,2,3) after the measurement of PWT and PWL.Their lumbar segments (L4,5)were removed for examination with transmission electron microscope and detection of Bcl-2 and caspase-3 expression (by immune-histochemistry).Results CCI significantly decreased PWT and PWL,increased Bcl-2 and caspase-3 expression at T1,2,3 and induced apoptosis in spinal dorsal horn neurons in group CCI as compared with group S.Intraperitoneal Dex significantly attenuated CCI-induced mechanical and thermal hyperalgesia and neuronal apoptosis in group D as compared with group CCI.Dex injected intraperitoneally further increased Bcl-2 expression but decreased caspase-3 expression in group D as compared with group CCI.Conclusion Reduction in neuronal apoptosis in spinal dorsal horn is involved in the attenuation of neuropathic pain by Dex.