Neurovascular damage in experimental allergic encephalomyelitis: a target for pharmacological control.
Neurovascular damage in experimental allergic encephalomyelitis: a target for pharmacological control.
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DOI：
10.1080/09629359791415
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发表时间：
1997
影响因子：
4.6
通讯作者：
Bolton C
中科院分区：
文献类型：
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作者：
Bolton C
血脑屏障（BBB）由连续的内皮层与紧密靠近的周细胞和星形胶质细胞组成，以提供对神经血管系统的稳态控制。人类脱髓鞘疾病多发性硬化症和动物对应的实验性过敏性脑脊髓炎（EAE）的特征在于增强的BBB渗透性，促进水肿形成和全身来源的炎症型细胞募集到靶组织中以介导最终的髓鞘损失和神经元功能障碍。EAE被认为是用于检查最终导致BBB完整性丧失的病理学的有用模型，并且该疾病现在被证明在评估化合物限制神经血管部位损伤的功效方面是有价值的。虽然几种潜在的破坏性介质已被牵连，并已被确定为在中枢神经系统的非疾病相关的条件下脑血管损伤的有效效应物，但最终导致EAE诱导的BBB崩溃的确切机制尚不清楚。审查认为，证据表明，共同的机制可能介导脑血管通透性的变化，无论最初的侮辱和讨论的治疗方法，控制血脑屏障泄漏的脱髓鞘疾病。
The blood-brain barrier (BBB) is composed of a continuous endothelial layer with pericytes and astrocytes in close proximity to offer homeostatic control to the neurovasculature. The human demyelinating disease multiple sclerosis and the animal counterpart experimental allergic encephalomyelitis (EAE) are characterized by enhanced permeability of the BBB facilitating oedema formation and recruitment of systemically derived inflammatory-type cells into target tissues to mediate eventual myelin loss and neuronal dysfunction. EAE is considered a useful model for examining the pathology which culminates in loss of BBB integrity and the disease is now proving valuable in assessing compounds for efficacy in limiting damage at neurovascular sites. The precise mechanisms culminating in EAE-induced BBB breakdown are unclear although several potentially disruptive mediators have been implicated and have been previously identified as potent effectors of cerebrovascular damage in non-disease related conditions of the central nervous system. The review considers evidence that common mechanisms may mediate cerebrovascular permeability changes irrespective of the initial insult and discusses therapeutic approaches for the control of BBB leakage in the demyelinating diseases.