汉防己甲素干预急性损伤脊髓神经元凋亡及bcl-2和bax表达:与甲基强的松龙的比较(英文)

Effects of tetrandrine on neuronal apoptosis,bcl-2 and bax expressions following acute spinal cord injury In comparison with methylprednisolone

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 demonstrated that tetrandrine has protection on acute spinal cord injury, but the specific mechanism remains poorly understood. OBJECTIVE： To study the protection of tetrandrine on rat acute spinal cord injury and to study its mechanism from apoptosis pathway. METHODS： A total of 100 rats were randomly divided into 4 groups. All rats were prepared for spinal cord injury models using modified Allen method except that in the sham-surgery group. Methylprednisolone and tetrandrine was injected into rats in the methylprednisolone and tetrandrine groups by tail intravenous injection prior to and at 24, 48 hours after model preparation. The same volume of physiological saline was injected in the sham-surgery and model groups. Basso-Beattie-Bresnahan （BBB score） was recorded at 8 hours, 1, 3, 7 and 14 days after model preparation. The morphological changes of spinal cord injury sites were observed by hematoxylin-eosin staining and the expressions of bcl-2 and bax were determined by immunohistochemistry. RESULTS AND CONCLUSION： The BBB score of methylprednisolone and tetrandrine groups were significantly higher than that model group at 7 and 14 days （P 0.05）, but there were no significant difference between the methylprednisolone group and tetrandrine group （P 0.05）. Hematoxylin-eosin staining showed that the spinal cord injured severely at 3-7 days, the injury degree in the methylprednisolone group and tetrandrine group was slighter than that of the model group, with smaller bax expression and greater bcl-2 expression （P0.01）. The findings demonstrated that, tetrandrine is able to protect neurons from apoptosis and promote the nerve function recovery by inhibiting the expression of Bax and promoting the expression of Bcl-2. Its effect is not inferior to methylprednisolone.