中国神经再生研究(英文版) ›› 2015, Vol. 10 ›› Issue (11): 1733-1734.doi: 10.4103/1673-5374.165288

• 观点:脑损伤修复保护与再生 • 上一篇    下一篇

共聚物-1治疗缺血性卒中可促进神经保护和神经发生 

  

  • 收稿日期:2015-08-03 出版日期:2015-12-07 发布日期:2015-12-07

Immunization with Cop-1 promotes neuroprotection and neurogenesis after ischemic stroke

Yolanda Cruz, Paola Suárez-Meade, Antonio Ibarra*   

  1. Facultad de Ciencias de la Salud, Universidad Anáhuac México Norte, Av. Universidad Anáhuac No. 46, Col. Lomas Anáhuac, C.P.52786, Huixquilucan Edo. de México, México (Cruz Y, Suárez-Meade P, Ibarra A)
    Proyecto CAMINA A.C., Tlalpan No. 4430 Col. Toriello Guerra, C.P. 14050, México City, México (Ibarra A)
  • Received:2015-08-03 Online:2015-12-07 Published:2015-12-07
  • Contact: Antonio Ibarra, Ph.D., iantonio65@yahoo.com;jose.ibarra@anahuac.mx.
  • Supported by:

    We thank Jorge Aguilar Cevallos for his assistance as style reviser and for her comments, which greatly improved this paper.

摘要:

脑卒中发生是由于脑血流的中断或干扰、氧和葡萄糖至神经组织的供应显著减少造成的。因此,几种细胞死亡机制(继发性损伤机制),例如坏死,兴奋性中毒,自由基产生和炎症都可催发病症。在过去的几十年里已经研究了各种具有溶栓、神经保护和修复性能的药物,然而,这些研究的结果似乎都不十分理想。因此,目前还没有一个完全有效的减少神经损伤的治疗方法。直到今天,一线脑卒中治疗方法仍是组织型纤溶酶原激活剂(tPA)。当施用时,它的溶栓特性可恢复血流。遗憾的是,tPA的治疗时间窗是非常短暂的,仅在缺血事件发生后的4.5小时内给药才会发生作用。共聚物-1是FDA已批准的用于治疗多发性硬化症的免疫调节药物,这意味着该药物的安全性已得到证实。作为一种治疗涉及炎症反应神经系统疾病的微创方法,共聚物-1具有调节炎症和增加局部神经营养因子产物的能力。初步研究数据使我们相信,共聚物-1的免疫活性通过诱导神经保护和神经修复可以增强功能恢复。这些有益效果通过避免自身免疫疾病、局部毒性和增加的神经营养因子水平来实现。作为FDA批准的治疗方法,共聚物-1可以易于应用在治疗临床脑血管疾病或认知障碍当中,以此降低死亡率并改善患者的生活质量。共聚物-1疗法代表了一种有希望的方法,应该可以在临床领域的神经退行性疾病中优化治疗策略。

Abstract:

A stroke occurs as a result of a disturbance or interruption of cerebral blood flow, significantly reducing the supply of oxygen and glucose to the neural tissue. Consequently, several cell death mechanisms (secondary lesion mechanisms) such as necrosis, excitotoxicity, free radical production and inflammation are trigerred. Over the last couple of decades, a variety of drugs with thrombolytic, neuroprotective, and restorative properties have been studied. However, the results of these studies appear to be limited. Thereby, there is not an entirely effective treatment for the reduction of neural damage. As of today, the first-line treatment for stroke is tissue plasminogen activator (tPA). When administered, its thrombolytic properties restore blood flow. Unfortunately; the therapeutic time window for tPA is very short, and its beneficial effects only appear if it is applied in less than 4.5 hours after an ischemic event. Innovative theurapeutic options are currently being developed in order to restore affected neuronal circuits following a cerebral ischemic event. Some of these innovative therapeutic approaches are based on stem cell transplantation and/or induction of neurogenesis. Cop-1 is an immunomodulatory drug already approved by the Food and Drug Administration (FDA) for the treatment of MS, implying that the safety of the drug has been validated. As a minimally invasive approach for treating neurological diseases involving an inflammatory response, Cop-1 has the ability to modulate inflammation and increase local neurotrophic factor production. Preliminary data has led us to believe that active immunization with Cop-1 enhances functional recovery by inducing neuroprotection and neurorestoration. These beneficial effects are achieved by avoiding autoimmune disease, local toxicity and by increasing the levels of neurotrophic factors. As an FDA-approved treatment, Cop-1 could easily be developed for treatment of clinical cerebrovascular diseases or cognitive disorders, with the objective of decreasing mortality and improving the quality of life of the patient. Therapy with Cop-1 represents a promising approach that should be explored in order to optimize the therapeutic strategy for neurodegenerative diseases in the clinical field.