Han Yuwei, Zhang Tingting, Su Jingyuan, Zhao Yuan, Li Xiaoming
Institute of Neurology, General Hospital of Shenyang Military Command, Shenyang, Liaoning 110016, China.
Institute of Neurology, General Hospital of Shenyang Military Command, Shenyang, Liaoning 110016, China.
J Clin Neurosci. 2017 Jun;40:157-162. doi: 10.1016/j.jocn.2017.03.003. Epub 2017 Mar 22.
Apigenin (API) is a naturally occurring plant flavone that exhibits powerful antioxidant and antiapoptosis. Oxidative stress plays an important role in the pathogenesis of early brain injury (EBI) following subarachnoid hemorrhage (SAH). The potential anti-oxidative and anti-apoptosis effects of API on EBI following SAH, however, have not been elucidated. The aim of this study was to assess whether API alleviates EBI after SAH via its anti-oxidative and anti-apoptotic effects. The endovascular puncture model was used to induce SAH and all the rats were subsequently sacrificed at 24h after SAH. Our data demonstrated that administration of API could significantly alleviate EBI (including neurological deficiency, brain edema, blood-brain barrier permeability, and cortical cell apoptosis) after SAH in rats. Meanwhile, API treatment reduced the reactive oxygen species (ROS) level and the concentration of malondialdehyde (MDA) and myeloperoxidase (MPO), elevated the ratio of glutathione (GSH) and oxidized glutathione (GSSG), and increased the amount of super-oxide dismutase (SOD) and hydrogen peroxide in brain cortex at 24h following SAH. Moreover, API treatment inhibited SAH-induced the expression of Bax and caspase-3, significantly reduced neuronal apoptosis. Collectively, API exerts its neuroprotective effect likely through the dual activities of anti-oxidation and anti-apoptosis, at least partly. These data provide a basic platform to consider API may be safely used as a potential drug for treatment of SAH.
芹菜素（API）是一种天然存在的植物黄酮，具有强大的抗氧化和抗凋亡作用。氧化应激在蛛网膜下腔出血（SAH）后的早期脑损伤（EBI）发病机制中起重要作用。然而，API对SAH后EBI的潜在抗氧化和抗凋亡作用尚未阐明。本研究的目的是评估API是否通过其抗氧化和抗凋亡作用减轻SAH后的EBI。采用血管内穿刺模型诱导SAH，所有大鼠在SAH后24小时处死。我们的数据表明，给予API可显著减轻大鼠SAH后的EBI（包括神经功能缺损、脑水肿、血脑屏障通透性和皮质细胞凋亡）。同时，API治疗降低了活性氧（ROS）水平、丙二醛（MDA）和髓过氧化物酶（MPO）的浓度，提高了谷胱甘肽（GSH）与氧化型谷胱甘肽（GSSG）的比值，并增加了SAH后24小时脑皮质中超氧化物歧化酶（SOD）和过氧化氢的含量。此外，API治疗抑制了SAH诱导的Bax和caspase-3的表达，显著减少了神经元凋亡。总体而言，API可能至少部分通过抗氧化和抗凋亡的双重作用发挥其神经保护作用。这些数据提供了一个基础平台，以考虑API可能作为治疗SAH的潜在药物安全使用。
