Sinensetin (SIN) is an important active compound that exists widely in citrus plants, and has been reported to exhibit various pharmacological properties, including anti-oxidative, anti-inflammatory, and anti-tumor. This study was designed to examine whether SIN can protect against amyloid beta (Aβ)-induced neurotoxicity and to elucidate the underlying mechanism. Our results showed that pretreatment with SIN for 1 h, followed by co-treatment with Aβ plus SIN for 24 h, attenuated Aβ25-35-induced cell viability reduction, oxidative stress, inflammation, and apoptosis in a dose-dependent manner. Aβ25-35-induced upregulation of Toll-like receptor 4 (TLR4) expression and nuclear translocation of nuclear factor-kappaB (NF-κB) p65 subunit were inhibited by pretreatment with SIN. Furthermore, the protective effect of SIN was abrogated by TLR4 overexpression. Hence, our data suggested that SIN attenuated Aβ25-35-induced neurotoxicity through the TLR4/NF-κB pathway.

中文翻译：

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Sinensetin 通过 TLR4/NF-κB 信号通路减弱 SH-SY5Y 细胞中淀粉样蛋白 Beta25-35 诱导的氧化应激、炎症和凋亡。

Sinensetin (SIN) 是一种重要的活性化合物，广泛存在于柑橘类植物中，据报道具有多种药理特性，包括抗氧化、抗炎和抗肿瘤。本研究旨在检查 SIN 是否可以防止淀粉样蛋白 β (Aβ) 诱导的神经毒性并阐明其潜在机制。我们的结果表明，用 SIN 预处理 1 小时，然后用 Aβ 加 SIN 共处理 24 小时，以剂量依赖性方式减弱 Aβ25-35 诱导的细胞活力降低、氧化应激、炎症和细胞凋亡。SIN 预处理可抑制 Aβ25-35 诱导的 Toll 样受体 4 (TLR4) 表达上调和核因子-κB (NF-κB) p65 亚基的核转位。此外，TLR4过表达消除了SIN的保护作用。因此，我们的数据表明 SIN 通过 TLR4/NF-κB 通路减弱 Aβ25-35 诱导的神经毒性。