β-七叶皂甙钠对脊髓损伤大鼠保护作用的实验研究被引量：2

Protection effects of sodium aescinate on the spinal cord nerve cell apoptosis in the early spinal cord injuried rats

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摘要目的探讨β-七叶皂甙钠(SA)对脊髓损伤(SCI)大鼠肢体功能及神经细胞凋亡的保护作用。方法采用改良Allen撞击方法建立SCI大鼠模型,随机将180只建模成功的SD大鼠按照数字随机表法分成对照组(等体积生理盐水腹腔注射)、SA组(5 mg/kg SA腹腔注射)及甲基强的松龙(MP)组(100 mg/kg MP腹腔注射),每组各60只。分别在治疗后8 h,1、4、7、14 d,利用斜板对双后肢瘫痪的恢复情况进行测定,并检测细胞凋亡的动态变化。结果随着观察时间的延长,各组大鼠后肢功能均有不同恢复,斜板角度逐渐增加。SA组和MP组治疗4 d后,大鼠后肢功能明显恢复,且呈时间依赖性(P<0.05)。治疗后8 h、1 d,对照组与SA组大鼠脊髓神经细胞凋亡指数高于MP组(P<0.05);治疗后4、7、14 d,SA组与MP组大鼠脊髓神经细胞凋亡指数低于对照组(P<0.05)。结论β-七叶皂甙钠对SCI大鼠肢体功能具有明显保护作用,其作用机理之一可能是通过减轻脊髓神经细胞凋亡来实现。 Objective To investigate the protection effects of sodium aescinate （SA） on the limb＇s function and nerve cell apoptosis in the early spinal cord injuried （SCI） rats. Methods To establish the rat model of SCI with modified Allen method, a total of 180 SD rats were randomly divided into control group （normal saline intraperitoneal injection）, SA group （5 mg/kg intraperitoneal injection of SA） and methylprednisolone （MP） group （100 mg/kg intraperitoneal injection of MP）, with 60 rats in each group. At 8 h, 1, 4, 7, 14 d after treatment, slope degree were determined to evaluate the improvement of the function of paralyzed hindlimb, then the injured segments were resected for pathylogical analysis Results With the observation time prolonged, hindlimb function of rats in each group recovered, the swash plate angle gradually increased. Hindlimb function recovered significantly at 4, 7, 14 d after the treatment in SA and MP groups （P 〈0.05）, and the time-dependent recovery could be investigated in two groups. At 8 h, 1 d after the treatment, apoptosis indexes of nerve cell of spinal cord in SA and control groups were higher than those in MP group （P 〈0.05）, while at 4, 7, 14 d after the treatment, apoptosis indexes in SA and MP goups were lower than those in control group （P 〈0.05）. Conclusion SA has protective effect on limb function of SCI rats, one of its mechanism of action is achieved by reducing apoptosis of spinal cord nerve cells.

作者丁勇吴玉杰傅智轶金文杰胡小鹏刘兴振

机构地区上海交通大学医学院附属第三人民医院骨科

出处《中国骨科临床与基础研究杂志》 2012年第6期441-445,共5页 Chinese Orthopaedic Journal of Clinical and Basic Research

基金上海交通大学医学院基金(10XJ22012)

关键词七叶素脊髓损伤细胞凋亡大鼠 Escin Spinal cord injury Apoptosis Rats

分类号 R285.5 [医药卫生—中药学]

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参考文献15

1Allen WE 3rd, D'Angelo CM, Kier EL. Correlation of micro- angiographic and electrophysiologic changes in experimental spinal cord trauma [J]. Radiography, 1974, 111(1): 107-115.
2Rivlin AS, Tator CH. Objective clinical assessment of motor function after experimental spinal cord injury in the rat [J]. J Neurosurg, 1977, 47(4): 577-581.
3Ekshyyan O, Aw TY. Apoptosis in acute and chronic neurological disorders [J]. Front Biosci, 2004, 9: 1567-1576.
4Kim DH, Vaccaro AR, Henderson FC, et al. Molecular biology of cervical myelopathy and spinal cord injury: role of oligodendrocyte apoptosis [J]. Spine J, 2012, 3(6): 510-519.
5Wu KL, Hsu C, Chan JY. Nitric oxide and superoxide anion differentially activate poly (ADP-ribose) polymerase-1 and Bax to induce nuclear translocation of apoptosis-inducing factor and mitochondrial release of cytochrome c after spinal cord injury [J]. J Neurotrauma, 2009, 26(7): 965-977.
6Wingrave JM, Sribnick EA, Wilford GG, et al. Relatively low levels of calpain expression in juvenile rat correlate with less neuronal apoptosis after spinal cord injury [J]. Exp Neurol, 2009, 187(2): 529-532.
7Yune TY, Kim S J, Lee SM, et al. Systemic administration of 17beta-estradiol reduces apoptotic cell death and improves functional recovery following traumatic spinal cord injury in rats [J]. J Neurotrauma, 2008, 21(3): 293-306.
8Barinaga M. New view of spinal cord injury [J] Science , 1996, 274(5292): 1466.
9Rezende AC, Vieira AS, Rogdrio F, et al. Effects of systemic administration of ciliary neurotrophie factor on Bax and Bcl-2 proteins in the lumbar spinal cord of neonatal rats after sciatic nerve transection [J]. Braz J Med Biol Res, 2008, 41 (11): 1024-1028.
10Fukaya C, Katayama Y, Kasai M, et al. Evaluation of time-dependent spread of tissue damage in experimental spinal cord injury by killed-end evoked potential: effect of high-dose methylprednisolone [J]. J Neurosurg, 2003, 98(1 Suppl): 56-62.

二级参考文献18

1Ramer MS,Harper GP,Bradbury EJ.Progress in spinal cord research-a refined strategy for the International Spinal Research Trust[J].Spinal Cord, 2000,38(8):449-472.
2Charriant C, Margaill,Represa A,et al.Apoptosis and necrosis after reversible focal ischemia: an in situ DNA fragementation analysis[J].J Cereb Blood Flow Metab,1996,16(2):186-194.
3Lee TT, Green BA. Advances in the management of acute spinal cord injury [J].Orthop Clin North Am,2002,33 (2):311-315.
4Goto T. Hoshino Y.Electmphysiological,histological and behavioral studies in a cat with acute compression of the spinal cord[J].J Orthop Sci,2001,6(1):59-67.
5Yong C, Arnold PM,Zoubine MN,et al.Apoptosis in cellular compartments of rats spinal cord after severe contusion injury[J]J Neurotrauma, 1998,15 (7):459-472.
6Sadowsky C,Volshteyn O,Schultz L.Spinal cord injury[J].Disabil Rehabil, 2002,24(13):680-687.
7Keane RW, Kraydieh S, Lotocki G,et al.Apoptotic and antiapoptotic mechanisms following spinal cord injury [J].JNeuropathol ExpNeurol, 2001,60(5):422-429.
8Blight AR,Zimber MP.Acute spinal cord injury:pharmacotherapy and drug development perspectives [J].Curr Opin Investig,2001,2(6) : 801-808.
9Kirshblum SC. Groah SL.,Spinal cord injury medicine Etiology,classification and acute medical management [J].Arch Phys Med Rehabil,2002 Mar,83(3 suppl 1):S50-57.
10Celik M,Gokmen N,Erbayraktar S,et al.Erythropoietin prevents motor neuron apoptosis and neurologic disability in experimental spinal cord ischemic injury [J].Proc Nail Acad Sci USA, 2002,1999(4):2258-2263.