Neurology:骨髓干细胞可以治疗中风
生物通 · 2014/04/15
2014年4月8日,在全球领先的临床神经病学杂志《Neurology》发表的一项研究中,美国科学家们证明,从骨髓中采集的干细胞可能对中风康复有益。


日前,加州大学欧文分校Sue & Bill Gross干细胞研究中心的科学家们证明,从骨髓中采集的干细胞可能对中风康复有益。

2014年4月8日,在全球领先的临床神经病学杂志《Neurology》发表的一项研究中,加州大学欧文分校Sue & Bill Gross干细胞研究中心的神经学家Steven Cramer博士和生物医学工程师赵伟安(Weian Zhao)进行了46项研究,在中风动物模型中检测了间充质干细胞(MSCs)——主要从骨髓中采集的一种多能成体干细胞类型——的应用情况。他们发现,在44项研究中骨髓间充质干细胞要明显优于对照治疗。

重要的是,不论剂量、相对应中风开始的MSCs服用时间或服用方式如何,这些细胞对功能康复的影响都很明显。(即使在中风后一个月服用,直接传到大脑或通过血管注射,这些细胞都起到帮助作用。

知名中风专家、神经学教授Cramer称:“中风是残疾的一个主要原因,我们为这些临床证据感到鼓舞,这些结果显示了MSCs对于缺血性脑卒中的疗效。我们对MSCs特别感兴趣,是因为它们来自于骨髓,是现成的,而且比较容易培养。此外,已有研究证明它们具有治疗其他疾病的价值。”

Cramer注意到,MSCs并不分化成神经细胞。通常,它们转化成各种各样的细胞类型,如骨细胞、软骨细胞和脂肪细胞。他指出:“但是它们的不可思议之处在于,它们就像一个可诱导的车轮上的药房,也是良好的免疫系统调节因子,而不是直接取代丢失大脑部分的细胞。”

在一项针对MSC作用机制的早期研究中,Cramer和赵博士综述了MSCs促进中风后大脑修复的方法。细胞被吸引到损伤部位,并响应这些损坏区域释放的信号,开始释放出各种不同的分子。以这种方式,MSCs精心安排了很多活动:生成血管以促进循环,保护开始死亡的细胞,脑细胞的生长等等。同时,当MSCs能够进入血液循环系统时,它们就停留在某些身体部位,这些部位可控制免疫系统,创造一种更利于脑修复的环境。

Cramer也是Sue&Bill Gross干细胞研究中心的医疗主任,他指出:“我们得出结论,在大多数动物研究中,MSCs可持续不断地改善多个疗效判定指标,具有非常大的效应量,因此对于进一步将MSCs用于人缺血性脑卒中的研究,这些结果奠定了一定的基础。”

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  • Meta-analysis of preclinical studies of mesenchymal stromal cells for ischemic stroke.

    Objectives: To evaluate the quality of preclinical evidence for mesenchymal stromal cell (MSC) treatment of ischemic stroke, determine effect size of MSC therapy, and identify clinical measures that correlate with differences in MSC effects. Methods: A literature search identified studies of MSCs in animal models of cerebral ischemia. For each, a Quality Score was derived, and effect size of MSCs was determined for the most common behavioral and histologic endpoints. Results: Of 46 studies, 44 reported that MSCs significantly improved outcome. The median Quality Score was 5.5 (of 10). The median effect size was 1.78 for modified Neurological Severity Score, 1.73 for the adhesive removal test, 1.02 for the rotarod test, and 0.93 for infarct volume reduction. Quality Score correlated significantly and positively with effect size for the modified Neurological Severity Score. Effect sizes varied significantly with clinical measures such as administration route (intracerebral > intra-arterial > IV, although effect size for IV was nonetheless very large at 1.55) and species receiving MSCs (primate > rat > mouse). Because many MSC mechanisms are restorative, analyses were repeated examining only the 36 preclinical studies administering MSCs ≥24 hours poststroke; results were overall very similar. Conclusions: In preclinical studies, MSCs have consistently improved multiple outcome measures, with very large effect sizes. Results were robust across species studied, administration route, species of MSC origin, timing, degree of immunogenicity, and dose, and in the presence of comorbidities. In contrast to meta-analyses of preclinical data for other stroke therapies, higher-quality MSC preclinical studies were associated with larger behavioral gains. These findings support the utility of further studies to translate MSCs in the treatment of ischemic stroke in humans.

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