Inhibition of neurogenic inflammation as a novel treatment for ischemic stroke.

Renée Turner, Robert Vink
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Abstract

Each year, 15 million people suffer a stroke, of which 5 million die and 5 million are left permanently disabled. Cerebral swelling is of particular concern following stroke as it accounts for much of the death and disability. However, the mechanisms leading to cerebral swelling are not yet fully understood. Recent studies from our laboratory suggest that neuropeptides, and specifically substance P, may be involved in the injury processes that occur following acute insults to the brain such as stroke and trauma, and may be responsible, in part, for edema formation. Levels of substance P are increased following CNS injury, indicative of neurogenic inflammation, and this is associated with injury to the blood-brain barrier, the development of cerebral edema, cell death and functional deficits. Subsequent studies inhibiting neuropeptide release have consistently shown decreased cerebral edema and improved neurological outcome, while substance P antagonists administered after the insult are efficacious in reducing post-stroke cerebral edema and neurological deficits. The current review summarizes the evidence supporting the benefits of inhibiting neurogenic inflammation to treat ischemic stroke.

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抑制神经源性炎症作为缺血性中风的新治疗方法。
每年有1500万人患中风,其中500万人死亡,500万人终身残疾。脑肿胀是中风后特别值得关注的问题,因为它是造成死亡和残疾的主要原因。然而,导致脑肿胀的机制尚不完全清楚。我们实验室最近的研究表明,神经肽,特别是P物质,可能参与脑急性损伤(如中风和创伤)后发生的损伤过程,并可能在一定程度上导致水肿的形成。中枢神经系统损伤后P物质水平升高,表明神经源性炎症,这与血脑屏障损伤、脑水肿的发展、细胞死亡和功能缺陷有关。随后的研究一致表明,抑制神经肽释放可减少脑水肿,改善神经系统预后,而P物质拮抗剂在脑损伤后给予治疗,可有效减少脑卒中后脑水肿和神经功能缺损。目前的综述总结了支持抑制神经源性炎症治疗缺血性卒中的益处的证据。
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