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背景:研究证实汉防己甲素对急性脊髓损伤有保护作用,但其具体机制尚不清楚。目的:观察汉防己甲素对急性脊髓损伤大鼠的神经保护作用,并从细胞凋亡通路探讨其作用机制。方法:将100只成年大鼠随机分为4组。采用加速压迫型Allen’s打击法制备脊髓损伤模型。甲强龙组和汉防己甲素组分别于造模前和造模后24,48h经尾静脉注射甲基强的松龙和汉防己甲素。假手术组与模型组注射等量生理盐水。造模后8h,1,3,7,14d采用BBB评分评估大鼠的运动功能,苏木精-伊红染色观察损伤脊髓组织的形态改变,免疫组织化学染色检测bcl-2和bax的表达。结果与结论:伤后7,14d,甲强龙组和汉防己甲素组大鼠的BBB评分显著高于模型组(P<0.05),各时间点甲强龙组和汉防己甲素组间BBB评分差异无显著性意义(P>0.05)。伤后3～7d,脊髓组织损伤最为严重,甲强龙组和汉防己甲素组的损伤程度较模型组轻,同时bax表达较模型组少,而bcl-2表达较模型组多(P<0.01)。说明汉防己甲素可通过增加bcl-2表达、降低bax表达,抑制急性脊髓损伤大鼠神经细胞凋亡,促进大鼠运动功能恢复,其作用不逊于甲基强的松龙。
BACKGROUND: Studies have shown that tetrandrine has a protective effect on acute spinal cord injury, but the exact mechanism is not clear. OBJECTIVE: To observe the neuroprotective effect of tetrandrine on acute spinal cord injury in rats and to explore its mechanism of action from the apoptotic pathway. Methods: 100 adult rats were randomly divided into 4 groups. Spinal cord injury model was prepared by accelerated compression Allen’s method. Methylprednisolone group and tetrandrine group were injected with methylprednisolone and tetrandrine at the tail vein 24 h and 48 h after modeling respectively. Sham operation group and model group were injected with normal saline. The BBB score was used to evaluate the motor function of rats at 8h, 1,3,7 and 14 days after modeling. Morphological changes of injured spinal cord were observed by hematoxylin-eosin staining. The expressions of bcl-2 and bax were detected by immunohistochemical staining. RESULTS AND CONCLUSION: At 7 and 14 days after injury, BBB scores of methylprednisolone group and tetrandrine group were significantly higher than that of model group (P <0.05). At each time point, BBB score difference was not significant (P> 0.05). The injury of spinal cord was the most serious from 3 to 7 days after injury. The damage of methylprednisolone and tetrandrine was lighter than that of the model group, while the expression of bax was less than that of the model group, while the expression of bcl-2 was more than that of the model group (P < 0.01). It suggested that tetrandrine could reduce the expression of bax and increase the expression of bcl-2, inhibit the apoptosis of nerve cells in rats with acute spinal cord injury, and promote the recovery of motor function in rats, which is no worse than that of methylprednisolone.