Ischemic stroke is the second most common cause of death worldwide and cerebral ischemia/reperfusion (I/R) injury also leads to serious tissue damage. Astilbin, a natural bioactive flavonoid compound, has been reported to have protective effects on neurological diseases. This study aims to investigate the effects of astilbin on cerebral I/R injury and determine the mechanisms involved. The results demonstrated that, in cerebral I/R rats, astilbin could attenuate I/R injury in the hippocampal region, decreasing the activity of lactate dehydrogenase (LDH) and malondialdehyde (MDA) in the rat brain. Astilbin also inhibited the I/R-induced upregulation of pro-inflammatory mediators (TNFα, IL-1β, IL-6). Similarly, in hypoxia/reperfusion (H/R) treated human neuroblastoma cells, astilbin could increase the cell viability of SH-SY5Y, decrease the activity of LDH and MDA, and inhibit the H/R-induced upregulation of pro-inflammatory mediators. For the mechanism study, western blot results indicated that astilbin could inhibit the expression of Toll-like receptor 4 (TLR4), myeloid differential protein 88 (MYD88) and phosphorylated NF-κB p65 in H/R treated SH-SY5Y cells. The research indicated that astilbin ameliorated cerebral I/R injury partly via the TLR4/MyD88/NF-κB pathway. Astilbin may have potential therapeutic effects on cerebral ischemia.

中文翻译：

---

落新妇苷通过抑制TLR4/MyD88/NF-κB通路减轻脑缺血/再灌注损伤

缺血性中风是全球第二大常见死亡原因，脑缺血/再灌注（I/R）损伤也会导致严重的组织损伤。据报道，落新妇苷是一种天然生物活性黄酮类化合物，对神经系统疾病具有保护作用。本研究旨在探讨落新妇苷对脑缺血再灌注损伤的影响并确定其机制。结果表明，在脑缺血再灌注大鼠中，落新妇苷可以减轻海马区缺血再灌注损伤，降低大鼠脑内乳酸脱氢酶（LDH）和丙二醛（MDA）的活性。Astilbin 还抑制 I/R 诱导的促炎介质（TNFα、IL-1β、IL-6）的上调。同样，在缺氧/再灌注（H/R）处理的人神经母细胞瘤细胞中，落新妇苷可以增加SH-SY5Y的细胞活力，降低LDH和MDA的活性，并抑制H/R诱导的促炎介质的上调。对于机制研究，蛋白质印迹结果表明，落新妇苷可以抑制 H/R 处理的 SH-SY5Y 细胞中 Toll 样受体 4 (TLR4)、髓样差异蛋白 88 (MYD88) 和磷酸化 NF-κB p65 的表达。研究表明落新妇苷部分通过TLR4/MyD88/NF-κB通路改善脑缺血再灌注损伤。落新妇苷可能对脑缺血具有潜在的治疗作用。