人参皂甙Rb1减轻大鼠脊髓缺血再灌注损伤的实验研究

目的在整体水平探讨人参皂甙Rb1对脊髓缺血再灌注损伤(spinal cord ischemiareperfusion injury,SCII)的治疗作用。方法 Sprague-Dawley(SD)大鼠72只,随机分为假手术组、对照组(SCII+安慰剂)和实验组(SCII+人参皂甙Rb1),采用腹主动脉夹闭法建立SCII模型。应用Basso-Beattie-Bresnahan(BBB)评分系统评价神经功能,HE染色观察病理组织结构和细胞形态改变,原位末端脱氧核苷酸转移酶标记(the in situ terminal deoxynucleotidyl transferase-mediateddUTP nick end-labeling technique,TUNEL)方法检测细胞凋亡情况。结果人参皂甙Rb1干预可以减轻脊髓缺血再灌注损伤导致的后肢功能障碍。HE染色显示人参皂甙Rb1干预可减轻神经元受损程度。TUNEL检测显示假手术组很少有细胞凋亡,对照组的神经细胞凋亡率最高,实验组与对照组比较可显著减少细胞凋亡率,差异有统计学意义(P<0.05)。结论人参皂甙Rb1可改善大鼠神经功能,减轻SCII导致的神经元受损,减少脊髓细胞凋亡。

Effects of Ginsenoside Rb1 on spinal cord ischemia-reperfusion injury of rats

Objective Determined the treatment effects of ginsenoside Rbl on spinal cord ischemia-reperfusion injury （SCII）. Methods Seventy-two Sprague-Dawley rats were randomly divided into 3 groups with 24 rats in each group. The groups were sham-operated group, SCII group （ control group）, ginsenoside Rbl-treated group （ experimental group）. The SCII models were established with the abdominal aortic clipping method. The nerve function was evaluated by Basso-Beattie- Bresnahan（BBB） scoring system, and the organizational structure and cell morphology were determined by HE staining. The apoptosis was detected by the in situ terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeLing technique （TUNEL）. Results After ginsenoside Rbl-treated, the BBB score was significantly higher than those of control group, the difference was statistically significant （ P 〈 0.05 ）. HE staining showd cell structure significmltly improved and nuclear struc- ture becomes clear after ginsenoside Rbl-treated. TUNEL study showed apoptosis was significantly increased of control group compared to sham-operated group, the difference was statistically significant （P 〈 0. 05 ）. Apoptosis rate of expenmental group was markedly lower than that of control group, the difference was statistically significant （P 〈 0. 05 ）. Conclusion Ginsen- oside Rbl can improve the nerve function of rats, and reduce nerve impairment and apoptosis caused by SCIL