N-乙酰半胱氨酸对大鼠脊髓损伤后运动功能恢复的影响及可能机制

Effect and possible mechanism of N-acetylcysteine on motor function of rats with spinal cord injury

目的观察N-乙酰半胱氨酸对大鼠脊髓损伤后运动功能恢复的影响,并探讨其可能的作用机制。方法健康成年Sprague-Dawley大鼠60只,随机分为N-乙酰半胱氨酸(N-acetylcysteine,NAC)治疗(NAC组)、单纯脊髓损伤组(SCI组)和假手术组(Sham组),每组20只。采用Allen法损伤大鼠T9脊髓节段,制备大鼠脊髓损伤动物模型。造模成功后15 min,NAC组腹腔注射NAC 150 mg/kg,每日1次,共7次;SCI组和Sham组腹腔注射等体积的生理盐水。于术后1 d、3 d、7d、14d随机抽取各组动物5只,进行后肢功能BBB评分、ELISA检测脊髓组织中炎症因子IL-1β和IL-18水平,Western blot检测脊髓组织中Caspase1蛋白表达水平。结果与Sham组比较,SCI组术后各时间点BBB评分均显著降低,脊髓组织中炎症因子IL-18和IL-1β水平均显著升高,Caspase1蛋白表达水平显著升高(<0.05)。与SCI组比较,NAC组术后3d、7d、14d BBB评分均显著升高,脊髓组织中IL-18和IL-1β水平显著降低,Caspase1表达水平显著降低(<0.05)。结论 NAC促进脊髓损伤大鼠运动功能的恢复可能与抑制Caspase1表达降低炎症因子IL-1β和IL-18水平相关。

Objective To study the effect and possible mechanism of N-acetylcysteine（NAC）on motor function of SD rats with spinal cord injury（SCI）. Methods 60 healthy adult SD rats were divided randomly into NAC group, Sham group and SCI group with 20 rats in each group. SCI model was made by Allen＇s mode at the level of the 9th thoracic vertebra, 15 rain later, NAC group was given 150 mg/kg NAC daily for 7 times by intraperitoneal injection, while SCI group and Sham group were given an equal volume of normal saline daily. The motor function was assessed by Basso-Beattie- Bresnahan （BBB） scale, the level of IL-1β and IL-18 in spinal cord was determined by ELISA and caspasel protein expression was determined by Western blot. Results Compared to Sham group, the BBB scores in SCI group were significantly increased, the level of IL-1β and IL-18 in spinal cord in SCI group was significantly increased, caspasel expression level in SCI group was also significantly increased （P〈0.05）. Compared to SCI group, BBB scores in NAC group were significantly increased, the level of IL-1β and IL-18 in NAC group was reduced at the 3rd, 7th and 14th days after SCI. Caspasel expression level in SCI group was also significantly downregulated（P〈0.05）. Conclusion The promotion of the motor function recovery in SCI rats by NAC might be related to the downregulation of inflammation.