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目的研究右美托咪定对神经病理性疼痛模型大鼠天门冬氨酸及白细胞介素1β(IL-1β)水平影响。方法用数字表法将96只健康成年雄性Wistar大鼠随机分为假手术组、模型组以及实验组,各24只;设置正常且不经任何处理的大鼠为空白组24只。模型组和实验组的大鼠暴露并结扎坐骨神经,建立神经病理性疼痛模型;假手术组仅暴露不结扎。实验组大鼠腹腔注射右美托咪定50μg·kg~(-1);假手术组、模型组大鼠腹腔注射等量生理盐水。用热刺痛仪测量各组大鼠的机械痛阈(MPT)、热痛阈(HPT)、天门冬氨酸及IL-1β水平变化。结果给药14 d后,假手术组的机械痛阈以及热痛阈分别为(19.99±2.07),(13.59±1.46)s,显著高于模型组的(9.92±1.12),(7.42±0.82)s,差异有统计学意义(P<0.05);空白组的机械痛阈以及热痛阈分别为(20.18±2.29),(14.39±1.55)s,显著高于模型组,差异有统计学意义(P<0.05);与模型组比较,实验组的机械痛阈以及热痛阈分别为(11.82±1.45),(8.79±0.93)s,显著升高,差异有统计学意义(P<0.05)。假手术组的天门冬氨酸及IL-1β分别为(12.38±1.44)μmol·mg~(-1)和(16.79±17.28)pg·mg~(-1),显著低于模型组的(15.93±1.82)μmol·mg~(-1)和(18.92±2.01)pg·mg~(-1),差异有统计学意义(P<0.05);空白组的天门冬氨酸及IL-1β分别为(6.19±0.73)μmol·mg~(-1)和(8.82±0.97)pg·mg~(-1),显著低于模型组,差异有统计学意义(P<0.05);实验组的天门冬氨酸及IL-1β分别为(9.82±1.02)μmol·mg~(-1)和(14.82±1.67)pg·mg~(-1),较模型组显著降低,差异有统计学意义(P<0.05)。结论右美托咪定可通过影响天门冬氨酸及IL-1β水平,实现镇痛的目的,同时抑制炎症反应,能够明显改善神经病理性疼痛。
Objective To investigate the effect of dexmedetomidine on aspartate and interleukin 1β (IL-1β) levels in neuropathic pain model rats. Methods Totally 96 healthy adult male Wistar rats were randomly divided into sham operation group, model group and experimental group, 24 rats in each group. Twenty-four rats in the normal control group and without any treatment were selected as blank control group. Rats in the model group and the experimental group were exposed and ligation of the sciatic nerve to establish a neuropathic pain model; sham operation group only exposed non-ligated. Rats in the experimental group were injected intraperitoneally with dexmedetomidine 50 μg · kg -1. Rats in the sham operation group and model group were intraperitoneally injected with normal saline. The mechanical pain threshold (MPT), heat pain threshold (HPT), aspartic acid and IL-1β levels in each group were measured with tachycardia. Results The mechanical and thermal pain thresholds in the sham group were (19.99 ± 2.07) and (13.59 ± 1.46) s, respectively, which were significantly higher than those in the model group (9.92 ± 1.12 and 7.42 ± 0.82) s, the difference was statistically significant (P <0.05). The mechanical pain threshold and thermal pain threshold in the blank group were (20.18 ± 2.29) and (14.39 ± 1.55) s, respectively, which were significantly higher than those in the model group (P <0.05). Compared with the model group, the mechanical pain threshold and the thermal pain threshold of the experimental group were (11.82 ± 1.45) and (8.79 ± 0.93) s, respectively, which were significantly increased (P <0.05). Aspartate and IL-1β were (12.38 ± 1.44) μmol · mg ~ (-1) and (16.79 ± 17.28) pg · mg ~ (-1) in sham operation group, which were significantly lower than those in model group (15.93 ± 1.82) μmol · mg -1 and (18.92 ± 2.01) pg · mg -1, respectively, with significant difference (P <0.05). Aspartate and IL-1β in the blank group were (6.19 ± 0.73) μmol · mg ~ (-1) and (8.82 ± 0.97) pg · mg ~ (-1), respectively, which were significantly lower than those in model group (P <0.05) (9.82 ± 1.02) μmol · mg ~ (-1) and (14.82 ± 1.67) pg · mg ~ (-1), respectively, which were significantly lower than those in model group (P < 0.05). Conclusion Dexmedetomidine can improve the neuropathic pain by affecting the level of aspartate and IL-1β, and achieve the purpose of analgesia and suppress the inflammatory reaction at the same time.