The highest disability rates and mortality among neurodegenerative diseases were caused by intracerebral hemorrhage (ICH). We previously proved that Benzene, 1,2,4-trimethoxy-5-(2-methyl-1-propen-1-yl) (BTY) has an inhibitory effect on sodium ion channel and an activation effect on GABA_A receptor, which were related to the brain injury. Based on this, we aimed to investigate BTY's neuroprotection on intracerebral hemorrhage and its underlying mechanism. In the in vivo study, a stereotactic injection of collagenase VII in Sprague Dawley rats (0.5 U) induced ICH and the BTY was intraperitoneally injected at 2 h after ICH. The neurological deficit scores, blood–brain barrier (BBB) permeability, and other indicators were assessed 24 h after ICH. The results showed that the BTY reduced brain edema and hematoma volume, improved neurological function and BBB permeability, and inhibited inflammatory factors and neuron apoptosis. The cell experiments proved that the BTY suppressed oxidative stress, cell apoptosis, intracellular calcium influx, and stabilized mitochondrial membrane potential by reducing glutamate's excitotoxicity. This study for the first time exhibited desirable neuroprotection of BTY, indicating it may be a promising neuroprotective agent for ICH therapy.

神经退行性疾病中最高的残疾率和死亡率是由脑出血 (ICH) 引起的。我们之前证明苯，1,2,4-三甲氧基-5-（2-甲基-1-丙烯-1-基）（BTY）对钠离子通道有抑制作用，对 GABA A 受体有激活作用_，从而与脑损伤有关。基于此，我们旨在探讨BTY对脑出血的神经保护作用及其机制。在体内研究中，在 Sprague Dawley 大鼠中立体定向注射胶原酶 VII (0.5 U) 诱导 ICH，并在 ICH 后 2 小时腹膜内注射 BTY。ICH 后 24 小时评估神经功能缺损评分、血脑屏障 (BBB) 通透性和其他指标。结果表明，BTY 可减轻脑水肿和血肿体积，改善神经功能和血脑屏障通透性，抑制炎症因子和神经元凋亡。细胞实验证明，BTY通过降低谷氨酸的兴奋性毒性来抑制氧化应激、细胞凋亡、细胞内钙内流和稳定线粒体膜电位。这项研究首次展示了 BTY 的理想神经保护作用，表明它可能是一种有前途的 ICH 治疗神经保护剂。