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首页 » 干细胞治疗 » Stem Cell Res & Ther:通过进行干细胞注射就可以改善大鼠的脊髓损伤状况

Stem Cell Res & Ther:通过进行干细胞注射就可以改善大鼠的脊髓损伤状况

来源:生物谷 2013-05-28 22:23

2013年5月28日 讯 /生物谷BIOON/ --近日,刊登在国际杂志Stem Cell Research & Therapy上的一篇研究报告中,来自美国加州大学圣地亚哥医学院的研究者通过研究揭示了,通过对大鼠进行单一性的人类神经干细胞注射就可以使其神经元再生以及改善神经元功能和急性脊髓损伤引发的运动损伤。

研究者Martin Marsala表示,通过将来自人类胎儿脊髓中的神经干细胞移植到大鼠的脊髓损伤部位就可以使大鼠产生一系列治疗效应,使得神经元间产生新的连接。在进行步行测试以及抑制肌肉痉挛状态的试验中,首先产生反应的是在对大鼠爪子的定位和控制上出现的;痉挛状态,即扩大的肌肉紧张以及不受控制的抽筋,其是一种常见的脊髓挫伤的表现。

所有的细胞移植动物都具有强大的接受移植物的能力,而且其可以促进人类神经元移植的神经元变得成熟。

小鼠损伤三天后接受纯的干细胞移植并且给予药物移植机体对外来干细胞的排除作用,研究者表示,损伤后的任何时间进行干细胞移植都可以阻断脊髓损伤腔的形成,但是需要进行更多的研究工作来确定时间对功能性神经学反应的影响。

进行干细胞移植需要注意两点,即刺激宿主神经元再生以及部分取代缺失神经元的功能。移植的骨髓干细胞是许多不同生长因子的丰富来源,这些生长因子可以起到神经保护的作用,并且可以促进宿主神经元神经纤维的生长。研究者在文中阐述了,移植的神经元可以产生同宿主神经元的信息交流,恢复损伤部位神经元中心的连接性。

研究者使用人类胚胎干细胞细胞系进行相关的研究,该细胞系已经获批进行慢性创伤性脊髓损伤病人的I期临床试验了。研究者的最终研究目的在于从病人机体诱导的多能干细胞中开发出神经前体细胞,即能够变成神经系统任何一种类型细胞能力的神经前体细胞,如果成功的话就可以消除病人进行免疫抑制疗法的需求了。

这篇文章的共同作者Joseph Ciacci表示,这项研究非常让人欣喜,因为这项研究为治疗急性脊髓损伤的病人的治疗提供了巨大的希望;如果前期研究是安全及有效的,而且移植入的细胞也具有活性,神经可以再生以及出现痉挛状态的减少,那么研究思路就将可以应用于其他严重类型的脊髓损伤病人的疗法中去。(生物谷Bioon.com)

Amelioration of motor/sensory dysfunction and spasticity in a rat model of acute lumbar spinal cord injury by human neural stem cell transplantation

Sebastiaan van Gorp, Marjolein Leerink, Osamu Kakinohana, Oleksandr Platoshyn, Camila Santucci, Jan Galik, Elbert A Joosten, Marian Hruska-Plochan, Danielle Goldberg, Silvia Marsala, Karl Johe, Joseph D Ciacci and Martin Marsala

Introduction Intraspinal grafting of human neural stem cells represents a promising approach to promote recovery of function after spinal trauma. Such a treatment may serve to: i) provide trophic support to improve survival of host neurons; ii) improve the structural integrity of the spinal parenchyma by reducing syringomyelia and scarring in trauma-injured regions; and iii) provide neuronal populations to potentially form relays with host axons, segmental interneurons, and/or alpha-motoneurons. Here we characterized the effect of intraspinal grafting of clinical grade human fetal spinal cord-derived neural stem cells (HSSC) on the recovery of neurological function in a rat model of acute lumbar (L3) compression injury. Methods Three-month-old female Sprague--Dawley rats received L3 spinal compression injury. Three days post-injury, animals were randomized and received intraspinal injections of either HSSC, media-only, or no injections. All animals were immunosuppressed with tacrolimus, mycophenolate mofetil, and methylprednisolone acetate from the day of cell grafting and survived for eight weeks. Motor and sensory dysfunction were periodically assessed using open field locomotion scoring, thermal/tactile pain/escape thresholds and myogenic motor evoked potentials. The presence of spasticity was measured by gastrocnemius muscle electromyography response during computer-controlled ankle rotation. At the end-point, gait (CatWalk), ladder climbing, and single frame analyses were also assessed. Syrinx size, spinal cord dimensions, and extent of scarring were measured by magnetic resonance imaging. Differentiation and integration of grafted cells in the host tissue were validated with immunofluorescence staining using human-specific antibodies. Results Intraspinal grafting of HSSC led to a progressive and significant improvement in lower extremity paw placement, amelioration of spasticity, and normalization in thermal and tactile pain/escape thresholds at eight weeks post-grafting. No significant differences were detected in other CatWalk parameters, motor evoked potentials, open field locomotor (Basso, Beattie, and Bresnahan locomotion score (BBB)) score or ladder climbing test. Magnetic resonance imaging volume reconstruction and immunofluorescence analysis of grafted cell survival showed near complete injury-cavity-filling by grafted cells and development of putative GABA-ergic synapses between grafted and host neurons. Conclusions Peri-acute intraspinal grafting of HSSC can represent an effective therapy which ameliorates motor and sensory deficits after traumatic spinal cord injury.s play a critical role in rVSV-mediated protection against ZEBOV.

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