CAJ | 학술논문

背景：研究证实脊髓损伤后早期应用甲基强的松龙冲击治疗可以减轻脊髓损伤的病理程度，但是近20年未再有突破性进展。 　　目的：观察β-七叶皂甙钠对脊髓损伤大鼠脊髓神经细胞坏死及胶质纤维酸性蛋白抗体表达的影响。 　　方法：采用改良Al en撞击方法建立脊髓损伤大鼠模型，将建模成功的180只SD大鼠按照随机数字表法分成3组，每组60只，造模后即刻给药，β-七叶皂甙钠组腹腔注射5 mg/kgβ-七叶皂甙钠，甲基强的松龙组腹腔注射100 mg/kg甲基强的松龙，对照组腹腔注射等体积生理盐水。每天给药1次，于治疗后8，24，96 h，治疗后7，14 d 5个时间节点处死实验动物并取损伤段脊髓进行苏木精-伊红染色及免疫组化染色观察脊髓组织坏死神经细胞数及胶质纤维酸性蛋白抗体表达情况。 　　结果与结论：各组均于治疗后8 h出现坏死细胞且7 d达高峰，14 d时水肿减轻但坏死细胞并未减少，但β-七叶皂甙钠及甲基强的松龙两组同一时间点上坏死细胞数目均明显少于对照组(P<0.05)；各组胶质纤维酸性蛋白吸光度均随着时间延长而增加，β-七叶皂甙钠组与对照组在96 h内增加快速，而甲基强的松龙组缓慢均匀增加，24 h以内β-七叶皂甙钠组与对照组之间无明显差别，但均低于甲基强的松龙组(P<0.05)，96 h后β-七叶皂甙钠及甲基强的松龙两组均明显低于对照组(P<0.05)，7 d后各组均开始缓慢下降。结果表明β-七叶皂甙钠对脊髓损伤大鼠脊髓细胞具有明显保护作用，可通过减少胶质纤维酸性蛋白的表达促进神经功能恢复，在用药2周时间内的效果与甲基强的松龙相似。
배경：연구증실척수손상후조기응용갑기강적송룡충격치료가이감경척수손상적병리정도，단시근20년미재유돌파성진전。 　　목적：관찰β-칠협조대납대척수손상대서척수신경세포배사급효질섬유산성단백항체표체적영향。 　　방법：채용개량Al en당격방법건립척수손상대서모형，장건모성공적180지SD대서안조수궤수자표법분성3조，매조60지，조모후즉각급약，β-칠협조대납조복강주사5 mg/kgβ-칠협조대납，갑기강적송룡조복강주사100 mg/kg갑기강적송룡，대조조복강주사등체적생리염수。매천급약1차，우치료후8，24，96 h，치료후7，14 d 5개시간절점처사실험동물병취손상단척수진행소목정-이홍염색급면역조화염색관찰척수조직배사신경세포수급효질섬유산성단백항체표체정황。 　　결과여결론：각조균우치료후8 h출현배사세포차7 d체고봉，14 d시수종감경단배사세포병미감소，단β-칠협조대납급갑기강적송룡량조동일시간점상배사세포수목균명현소우대조조(P<0.05)；각조효질섬유산성단백흡광도균수착시간연장이증가，β-칠협조대납조여대조조재96 h내증가쾌속，이갑기강적송룡조완만균균증가，24 h이내β-칠협조대납조여대조조지간무명현차별，단균저우갑기강적송룡조(P<0.05)，96 h후β-칠협조대납급갑기강적송룡량조균명현저우대조조(P<0.05)，7 d후각조균개시완만하강。결과표명β-칠협조대납대척수손상대서척수세포구유명현보호작용，가통과감소효질섬유산성단백적표체촉진신경공능회복，재용약2주시간내적효과여갑기강적송룡상사。
BACKGROUND:The methylprednisolone pulse therapy in early period of spinal cord injury can attenuate the pathological degree of spinal cord injury, however no breakthrough was found within recent 20 years. OBJECTIVE:To observe the protection effects of sodium aescinate on the nerve cellapoptosis and expression of glial fibrial ary acidic protein (GFAP) in the early spinal cord injured rats. METHODS:Spinal cord injury models were established with the modified Al en’s method in 180 Sprague-Dawley rats, and were randomly divided into three groups, with 60 rats in each group. Immediately after injury, the rats in three groups were intraperitoneal y injected with sodium aescinate (5 mg/kg), methylprednisolone (100 mg/kg) and equal saline, respectively, once per day. At 8 hours, 24 hours, 96 hours and 7 days, 14 days after injury, rats were sacrificed and the injured segments were resected for hematoxylin-eosin staining and immunohistochemical staining, the nerve cellapoptosis and GFAP expression were detected. RESULTS AND CONCLUSION:The apoptotic nerve cells were seen at 8 hours after injury and the number of apoptotic cells reached the peak at 7 days, the edema was attenuated at 14 days without less nerve cellapoptosis in al groups, significantly fewer apoptotic nerve cells can be seen in sodium aescinate and methylprednisolone groups compared with the control group (P<0.05) at each time. The expression of GFAP was increased in the time dependant manner in al groups, the increase was slow in methylprednisolone group but sharp in sodium aescinate group and control group within 96 hours. There was no difference between control group and sodium aescinate group within 24 hours (P>0.05), which was lower than methylprednisolone group (P<0.05);after 96 hours, methylprednisolone group and sodium aescinate group were both significantly lower than control group (P<0.05). Furthermore, the decreasing expression was observed in al groups after 7 days. Sodium ascinate has obvious protection effects on nerve cells in spinal cord injured rats and promotes neurological function through decreasing GFAP expression after injury. The efficacy of sodium ascinate is equal to that of methylprednisolone within 2 hours.