上海交通大学学报（医学版）

上海交通大学学报（医学版） ›› 2017, Vol. 37 ›› Issue (12): 1594-.doi: 10.3969/j.issn.1674-8115.2017.12.003

• 论著（基础研究） • 上一篇    下一篇

鱼腥草素钠对大鼠脊髓损伤神经元的影响

唐维 1，夏永智 1，刘敬贤 1，刘露 2，晏怡 1   

  1. 重庆医科大学附属第一医院 1. 神经外科，2. 烧伤整形外科，重庆 400016
  • 出版日期:2017-12-28 发布日期:2018-01-10
  • 通讯作者: 晏 怡，电子信箱：yanyi2005@vip.sina.com。
  • 作者简介:唐 维（1989—），男，硕士生；电子信箱：1151914710@qq.com。
  • 基金资助:
     国家自然科学基金（81100906）；国家临床重点专科建设项目（财社 [2011]170 号）；重庆市自然科学基金（cstc2012jjA10055）

Effects of sodium houttuyfonate on spinal cord injured neurons in rats

TANG Wei1, XIA Yong-zhi1, LIU Jing-xian1, LIU Lu2, YAN Yi1 #br#   

  1. 1. Department of Neurosurgery, 2. Department of Burn and Plastic Surgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China
  • Online:2017-12-28 Published:2018-01-10
  • Supported by:
    National Natural
    Science Foundation of China, 81100906; National Clinical Key-Discipline Construction Program of China, [2011] 170; Natural Science Foundation of Chongqing Municipality,
    cstc2012jjA10055

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摘要： [ 摘要 ] 目的 · 探究鱼腥草素钠（SH）对大鼠脊髓外伤（TSCI）早期神经元的影响及其机制。方法 · 随机将 40 只成年雌性大鼠分为假手术组（n=8）、对照组（n=8）和实验组（n=24）。假手术组仅打开椎板，但不做脊髓钳夹；其余 2 组均做脊髓钳夹。实验组于术后 1 h 用 SH 干预，根据剂量不同分为低 [0.06 g/(kg · d)]、中 [0.12 g/(kg · d)]、高 [0.24 g/(kg · d)] 剂量组，假手术组及对照组给予等量生理盐水，连续 3 d 灌胃给药。以大鼠 BBB 评分及尼氏染色作为标准，筛选 SH 的最佳治疗剂量。为探讨 SH 神经元保护的可能机制，随机将 72 只大鼠分为假手术组、对照组、SH 最佳剂量组，各 24 只，术后干预同前；免疫荧光和免疫组织化学分别检测前角运动神经元及 cleaved-caspase3 阳性神经元，Western blotting 检测 NeuN、Bax、Bcl-2、cleaved-caspase3 的表达。结果 · 术后 5 d 和 7 d，SH 低剂量组 BBB 评分均低于中、高剂量组（均 P<0.01），但高于对照组（均 P<0.01）；中、高剂量组 BBB 评分无显著差异。术后7 d，低剂量组及对照组尼氏体较中、高剂量组崩解破裂增多，数量减少，着色淡；但中、高剂量组尼氏染色结果无差异。综合 BBB评分及尼氏染色结果，判定本实验 SH 的最佳治疗剂量为 0.12 g/(kg · d)。在最佳剂量干预下，术后 3 d 和 7 d，前角运动神经元数量、NeuN 及 Bcl-2 的表达量均多于对照组（均 P<0.01）；前角 cleaved-caspase3 阳性神经元数目、Bax 及 cleaved-caspase3 的表达则相反（均 P<0.01）。结论 · SH 对 TSCI 后神经元具有一定保护作用，其机制可能是上调 Bcl-2/ Bax 的比值，减少神经元的凋亡。

关键词: &ensp, 脊髓损伤；鱼腥草素钠；神经元；凋亡

Abstract:

[Abstract] Objective · To investigate the effects of sodium houttuyfonate (SH) on neurons in early traumatic spinal cord injury (TSCI) rats and its
mechanism. Methods · Forty adult female rats were randomly divided into sham group (n=8), control group (n=8) and experimental group (n=24). The
sham group only received opened laminectomy without spinal cord clamping, the spinal cords in other two groups were clamped. The experimental group
was divided into low [0.06 g/(kg·d)], moderate [0.12 g/(kg·d)] and high [0.24 g/(kg·d)] dose subgroups, in which SH was administrated intragastrically 1 h
after operation and next two days. The other groups were given equivalent normal saline. The best therapeutic dose of SH was screened out by the results
of the BBB scores and Nissl staining. To explore the neuroprotection mechanisms of SH, 72 rats were randomly divided into sham group (n=24), model
group (n=24) and SH best dose group (n=24), the postoperative interventions were as same as above. Immunofluorescence and immunohistochemistry
were respectively used to detect the number of motor neurons and cleaved-caspase3 positive staining neurons, the expression of Bax, Bcl-2, NeuN and
cleaved-caspase3 was detected by Western blotting. Results · The BBB scores on day 5 and day 7 after operation in low dose group were higher than
those of control group (all P<0.01), but lower than those of moderate and high dose groups (all P<0.01), and the scores in the moderate and high dose
groups were not different significantly. On day 7 after operation, compared with moderate and high dose groups, the dissolution of Nissl bodies in low
dose group and control group increased, the number of Nissl bodies reduced, and the colour shallowed. But Nissl staining in moderate and high dose groups were similar. The optimal dose of SH was 0.12 g/(kg·d), which was judged by the results of BBB scores and Nissl staining. On day 3 and day 7 after operation, compared with control group, the number of motor neurons and the expression of NeuN and Bcl-2 in SH best dose group were increased (all P<0.01), while the number of cleved-caspase3 positive staining neurons and the expression of Bax and cleaved-caspase3 were reduced (all P<0.01). Conclusion · SH has a certain neuroprotection on neurons in TSCI, its mechanism may be through upregulating the ratio of Bcl-2/Bax, thereby reducing the neuronal apoptosis.

Key words: spinal cord injury, sodium houttuyfonate, neuron, apoptosis