Proteimax Biotechnology, 05581001, São Paulo, Brazil.
Special Laboratory of Pain and Signaling, Butantan Institute, São Paulo, 05503-900, Brazil.
Neurosci Lett. 2020 Mar 16;721:134765. doi: 10.1016/j.neulet.2020.134765. Epub 2020 Jan 28.
Previous studies suggested the pharmacological potential of rat hemopressin (PVNFKFLSH) and its shorter synthetic peptide NFKF, to protect from pilocarpine-induced seizures in mice. Orally administered NFKF was shown to be hundred times more potent than cannabidiol in delaying the first seizure induced by pilocarpine in mice. Here, using an experimental autoimmune encephalomyelitis (EAE) model of multiple sclerosis we have shown that C57BL/6 J mice orally administrated with NFKF (500 μg/kg) presented better EAE clinical scores and improved locomotor activity compared to saline administrated control mice. NFKF blocked the production of IL-1beta and IL-6, and has high scores binding cannabinoid type 2 receptors. Therefore, NFKF is an exciting new possibility to neurodegenerative diseases therapeutics.
先前的研究表明,鼠血红蛋白缩氨酸(PVNFKFLSH)及其较短的合成肽 NFKF 具有药理学潜力,可保护小鼠免受匹罗卡品诱导的癫痫发作。已证明口服给予 NFKF 比大麻素在延迟匹罗卡品诱导的小鼠首次癫痫发作方面有效一百倍。在这里,我们使用多发性硬化症的实验性自身免疫性脑脊髓炎 (EAE) 模型表明,与给予生理盐水的对照小鼠相比,用 NFKF(500μg/kg)口服给予的 C57BL/6 J 小鼠呈现出更好的 EAE 临床评分和改善的运动活性。NFKF 阻断了 IL-1beta 和 IL-6 的产生,并且对大麻素 2 型受体具有高结合评分。因此,NFKF 是神经退行性疾病治疗的一个令人兴奋的新可能性。