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J Biol Res (Thessalon). 2019 Nov 12;26:15. doi: 10.1186/s40709-019-0102-1. eCollection 2019 Dec.

Tanshinone IIA attenuates Aβ-induced neurotoxicity by down-regulating COX-2 expression and PGE2 synthesis via inactivation of NF-κB pathway in SH-SY5Y cells.

Author information

1
Department of Neurology, Huaihe Hospital of Henan University, No. 357 Ximen Street, Kaifeng, 475000 China.

Abstract

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.

KEYWORDS:

Alzheimer’s disease; Amyloid-β; COX-2; NF-κB pathway; PGE2; Tanshinone IIA

Conflict of interest statement

Conflicts of interestsThe authors declare that they have no competing interests.

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