Amyloid-β (Aβ)-induced neurotoxicity is a major pathological mechanism of Alzheimer’s disease (AD). Tanshinone IIA (Tan IIA), extracted from traditional Chinese herb Radix salvia miltiorrhiza, possesses anti-oxidant and anti-inflammatory actions, as well as neuroprotective effects. The present study aims to explore the possible mechanism by which Tan IIA attenuated Aβ-induced neurotoxicity. Exposure of SH-SY5Y cells to different concentrations of Aβ led to neurotoxicity by reducing cell viability, inducing cell apoptosis and increasing neuroinflammation in a dose-dependent manner. Moreover, Aβ treatment promoted cyclooxygenase-2 (COX-2) expression and Prostaglandin E2 (PGE2) secretion, and activated nuclear transcription factor kappa (NF-κB) pathway in SH-SY5Y cells. However, pretreatment of SH-SY5Y cells with Tan IIA prior to Aβ prevented these Aβ-induced cellular events noticeably. These data suggested that Tan IIA exerted its neuroprotective action by alleviating Aβ-induced increase in COX-2 expression and PGE2 secretion via inactivation of NF-κB pathway.

中文翻译：

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丹参酮IIA通过失活SH-SY5Y细胞中的NF-κB通路而下调COX-2表达和PGE2合成，从而减轻Aβ诱导的神经毒性。

淀粉样β（Aβ）诱导的神经毒性是阿尔茨海默氏病（AD）的主要病理机制。丹参酮IIA（Tan IIA）是从中草药丹参中提取的，具有抗氧化和抗炎作用，并具有神经保护作用。本研究旨在探讨Tan IIA减弱Aβ诱导的神经毒性的可能机制。SH-SY5Y细胞暴露于不同浓度的Aβ会导致神经毒性，其方式是降低细胞活力，诱导细胞凋亡并以剂量依赖性方式增加神经炎症。此外，Aβ处理促进了SH-SY5Y细胞中环氧合酶2（COX-2）的表达和前列腺素E2（PGE2）的分泌，并激活了核转录因子kappa（NF-κB）途径。然而，在Aβ之前用Tan IIA预处理SH-SY5Y细胞可明显防止这些Aβ诱导的细胞事件。这些数据表明，Tan IIA通过使Aβ诱导的NF-κB通路失活减轻COX-2表达和PGE2分泌的增加而发挥其神经保护作用。