Giacoppo Sabrina, Galuppo Maria, De Nicola Gina Rosalinda, Iori Renato, Bramanti Placido, Mazzon Emanuela
IRCCS Centro Neurolesi "Bonino-Pulejo", Via Provinciale Palermo, contrada Casazza, 98124, Messina, Italy.
Consiglio per la ricerca in agricoltura e l'analisi dell'economia agraria, Centro di ricerca per le colture industriali (CRA-CIN), Via di Corticella 133, 40128, Bologna, Italy.
BMC Complement Altern Med. 2015 Nov 6;15:397. doi: 10.1186/s12906-015-0929-4.
Cerebral ischemia and reperfusion (CIR) is a pathological condition characterized by a first blood supply restriction to brain followed by the consequent restoration of blood flow and simultaneous reoxygenation. The aim of this study was to evaluate the neuroprotective effects of Tuscan black kale sprout extract (TBK-SE) bioactivated with myrosinase enzyme, assessing its capability to preserve blood-brain barrier (BBB), in a rat model of CIR.
CIR was induced in rats according to a classic model of carotid artery occlusion for a time period of 1 h and the reperfusion time was prolonged for seven days.
By immunohistochemical evaluation and western blot analysis of brain and cerebellum tissues, our data have clearly shown that administration of bioactive TBK-SE is able to restore alterations of tight junction components (claudin-5 immunolocalization). Also, bioactive TBK-SE reduces some inflammatory key-markers (p-selectin, GFAP, Iba-1, ERK1/2 and TNF-α), as well as the triggering of neuronal apoptotic death pathway (data about Bax/Bcl-2 balance, p53 and cleaved-caspase 3) and the generation of radicalic species by oxidative stress (results focused on iNOS, nitrotyrosine and Nrf2).
Taken together, our findings lead to believe that bioactive TBK-SE exerts pharmacological properties in protecting BBB integrity through a mechanism of action that involves a modulation of inflammatory and oxidative pathway as well into control of neuronal death.
脑缺血再灌注(CIR)是一种病理状态,其特征是大脑首先出现血液供应受限,随后血流恢复并同时重新供氧。本研究的目的是评估经黑芥子酶生物活化的托斯卡纳黑羽衣甘蓝芽提取物(TBK-SE)的神经保护作用,在CIR大鼠模型中评估其保护血脑屏障(BBB)的能力。
根据经典的颈动脉闭塞模型在大鼠中诱导CIR,持续1小时,再灌注时间延长7天。
通过对脑和小脑组织的免疫组织化学评估和蛋白质印迹分析,我们的数据清楚地表明,给予生物活性TBK-SE能够恢复紧密连接成分的改变(claudin-5免疫定位)。此外,生物活性TBK-SE还能降低一些炎症关键标志物(p-选择素、GFAP、Iba-1、ERK1/2和TNF-α),以及神经元凋亡死亡途径的触发(关于Bax/Bcl-2平衡、p53和裂解的半胱天冬酶3的数据)和氧化应激产生的自由基(结果集中在诱导型一氧化氮合酶、硝基酪氨酸和核因子E2相关因子2)。
综上所述,我们的研究结果使我们相信,生物活性TBK-SE通过一种作用机制发挥药理特性,该机制涉及调节炎症和氧化途径以及控制神经元死亡,从而保护BBB的完整性。