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丹参注射液椎管内局部灌注对急性脊髓损伤的保护作用 被引量:9

Experimental study on the protective effect of Danshen perfused through subarachnoid space on acute injury of spinal curd in rabbits
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摘要 目的 探讨丹参对急性脊髓损伤的防治作用。方法 以改良Allen's法造成兔不完全性脊髓损伤的模型,硬膜下插管。随机分成丹参治疗组和对照组。术后按每天0.3ml/kg体重的总量分4次从硬膜下导管推入丹参注射液,对照组推入生理盐水。损伤后8、72h对脊髓损伤区进行过氧化物歧化酶(SOD)、丙二醛(MDA)、组织形态学观察、神经元凋亡、bcl-2等进行评价。结果 丹参组SOD含量高于对照组(P<0.01),MDA含量低于对照组(P<0.01)。细胞凋亡数目TUNEL法丹参组低于对照组(P<0.01),流式细胞术检测凋亡丹参组低于对照组(P<0.05)。bcl-2的表达丹参组高于对照组(P<0.05)。神经元及神经纤维变性、坏死轻于对照组。结论 丹参能改善损伤脊髓微循环,抑制和减轻脊髓损伤后的两种死亡方式坏死和凋亡。 Objective To study the protective effect of Danshen on the acute spinal cord injury. Methods Forty-eight rabbits with spinal cord incomplete injury by modified Allen's crush method were randomly divided into control group and Danshen group. Danshen or NS of 0.3 ml. kg^(-1). day was respectively supplied through subarachnoid cavity postoperatively. The contents of SOD and MDA in spinal tissue were determined, and morphological changes of spinal cord were observed. The cell apoptosis was examined and the expression of bel-2 was detected immunohistochemically 8 and 72 h post-operatively. Result In Danshen group, the content of SOD was higher, while that of MDA was lower than in the control group (both P<0.01 ). The number of apoptotic neurons was significantly less in Danshen group than that in the control group by TUNEL (P<0.01) and flow cytometry (P<0.05). The number of bcl-2 protein expression positive cells was more in Danshen group than in the control group (P<0.05), and the degeneration of neurons and neurofibril was milder than in the control group. Conlusion Danshen could protect neurons and decrease the apoptosis of neurons. Danshen can improve the microcirculation of spinal cord.
出处 《中华实验外科杂志》 CAS CSCD 北大核心 2004年第8期993-994,共2页 Chinese Journal of Experimental Surgery
基金 湖北省重点科技发展计划项目(20002P1713)
关键词 对照组 丹参注射液 急性脊髓损伤 局部灌注 椎管内 硬膜下 坏死 变性 SOD 数目 Spinal cord injury Danshen Neurons Apoptosis Subarechnoid space
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参考文献1

  • 1Dumont RJ,Okonkwo DO,Verma S,et al.Acute spinal cord injury, part I: pathophysiologic mechanisms[].Clinical Neurophysiology.2001

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