HLDF-6肽羧酸和酰胺形式的比较研究:对缺血性脑卒中动物模型的神经保护和益智作用

Аnna P Bogachuk, Z. Storozheva, A. Proshin, V. V. Sherstnev, Irina V. Smirnova, T. Shuvaeva, V. Lipkin
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引用次数: 1

摘要

脑血管疾病是现代世界最紧迫的医疗和社会问题之一。与循环功能不全相关的神经系统疾病的患病率高达人口的20%,并且呈上升趋势。许多神经系统疾病的特点是病程持续严重,持续的功能缺陷导致有限或完全残疾。缺血性脑卒中是最严重的脑血管疾病之一。脑缺血条件下脑组织损伤发展的机制需要引入一种称为神经保护的特殊治疗。神经保护旨在阻断细胞死亡的延迟机制——氧化应激、细胞因子失衡、局部层压、营养功能障碍和细胞凋亡。神经组织死亡的所有机制之间的紧密联系激发了调节效应的开发,可以通过刺激调节系统来实现。多肽是调控过程中的关键参与者之一。治疗IS和其他脑部疾病的最佳方案应该包括同时影响疾病发病机制中几个关键组成部分的药物的应用。对这些化合物的另一个重要要求是在用于长期预防性治疗时没有毒性作用。由于摘要
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Comparative study of carboxylate and amide forms of HLDF-6 peptide: Neuroprotective and nootropic effects in animal models of ischemic stroke
Cerebrovascular diseases are among the most urgent medical and social problems of the modern world. The prevalence of nervous system diseases associated with circulatory insuf iciency is up to 20% of the population and is trending upwards. Many nervous system diseases are characterized by a lingering severe course and persistent functional defects resulting in limited or total disability [1]. One of the most severe cerebrovascular diseases is ischaemic stroke (IS). Mechanisms of brain tissue damage development under conditions of cerebral ischaemia necessitate the introduction of a special type of therapy known as neuroprotection. Neuroprotection is aimed at interrupting the delayed mechanisms of cell death—oxidative stress, cytokine imbalance, local in lammation, trophic dysfunction, and apoptosis. A tight interconnection between all mechanisms of nervous tissue death motivates exploitation of the modulating effect that could be achieved through stimulation of the regulatory systems. Peptides are among the key players in regulatory processes [2]. An optimal scenario of therapy for IS and other cerebral disorders should comprise the application of agents simultaneously affecting several key components in the pathogenesis of the disease. Another important requirement for these compounds is the absence of toxic effects when used for prolonged preventive treatment. Due to Abstract
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