从神经炎症的角度看慢性脑缺血药物治疗的新前景

I. N. Samartsev, S. A. Zhivolupov
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引用次数: 1

摘要

世界范围内卒中的高患病率要求对脑血管疾病患者管理的现代学说进行修订。显然,仅仅积极地改变血管病理的危险因素并不能保证预防急性脑血管意外,这是脑血管疾病的中间或最终阶段。在这方面,使用神经保护剂,包括长春西汀,可以增加脑组织对缺氧的耐受性。长春西汀是长春胺生物碱的衍生物,具有抑制磷酸二酯酶和电压依赖性Na+通道的作用,在许多国家广泛用于治疗包括慢性脑缺血在内的脑血管疾病。最近的研究发现了长春西汀的一些新的治疗作用,包括通过脑源性神经营养因子刺激神经可塑性和抑制神经炎症。后一种机制是通过NF-kB抑制NF-kB依赖性促炎分子的表达,阻止NLRP3炎性小体的形成而介导的。新的数据允许重新考虑长春西汀在预防和治疗脑血管疾病中的地位,并推荐其在广泛的慢性脑缺血患者中使用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
New prospects for drug treatment of chronic cerebral ischemia from the standpoint of neuroinflammation
The high prevalence of stroke worldwide requires a revision of the modern doctrine of the management of patients with cerebrovascular disease. It is obvious that only aggressive modification of risk factors for vascular pathology does not guarantee the prevention of acute cerebrovascular accident, which is an intermediate or final stage of cerebrovascular disease. In this regard, the use of neuroprotectors, including vinpocetine, can increase the tolerance of brain tissue to hypoxia. Vinpocetine, a derivative of the alkaloid vincamine, inhibiting phosphodiesterase and voltage-dependent Na+- channels is widely used in many countries for the treatment of cerebrovascular diseases, including chronic cerebral ischemia. Recent studies have identified a number of new therapeutic effects of vinpocetine, including stimulation of neuroplasticity via brain-derived neurotrophic factor and inhibition of neuroinflammation. The latter mechanism is mediated by the effect on NF-kB that suppresses the expression of NF-kBdependent pro-inflammatory molecules and prevents the formation of NLRP3 inflammasome. New data allow to reconsider the place of vinpocetine in the prevention and treatment of cerebrovascular disorders, and to recommend its use in a wide range of patients with chronic cerebral ischemia.
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