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

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 pres...

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Main Authors:	Lijiao Geng, Wei Liu, Yong Chen
Format:	Article
Language:	English
Published:	BMC 2019-11-01
Series:	Journal of Biological Research - Thessaloniki
Subjects:	Tanshinone IIA Amyloid-β COX-2 PGE2 NF-κB pathway Alzheimer’s disease
Online Access:	http://link.springer.com/article/10.1186/s40709-019-0102-1

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record_format	Article
spelling	doaj-c45de657148e4b12b7291da7ee3ed8d12020-11-25T03:58:35ZengBMCJournal of Biological Research - Thessaloniki2241-57932019-11-0126111010.1186/s40709-019-0102-1Tanshinone IIA attenuates Aβ-induced neurotoxicity by down-regulating COX-2 expression and PGE2 synthesis via inactivation of NF-κB pathway in SH-SY5Y cellsLijiao Geng0Wei Liu1Yong Chen2Department of Neurology, Huaihe Hospital of Henan UniversityDepartment of Neurology, Huaihe Hospital of Henan UniversityDepartment of Neurology, Huaihe Hospital of Henan UniversityAbstract 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.http://link.springer.com/article/10.1186/s40709-019-0102-1Tanshinone IIAAmyloid-βCOX-2PGE2NF-κB pathwayAlzheimer’s disease
collection	DOAJ
language	English
format	Article
sources	DOAJ
author	Lijiao Geng Wei Liu Yong Chen
spellingShingle	Lijiao Geng Wei Liu Yong Chen 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 Journal of Biological Research - Thessaloniki Tanshinone IIA Amyloid-β COX-2 PGE2 NF-κB pathway Alzheimer’s disease
author_facet	Lijiao Geng Wei Liu Yong Chen
author_sort	Lijiao Geng
title	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
title_short	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
title_full	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
title_fullStr	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
title_full_unstemmed	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
title_sort	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
publisher	BMC
series	Journal of Biological Research - Thessaloniki
issn	2241-5793
publishDate	2019-11-01
description	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.
topic	Tanshinone IIA Amyloid-β COX-2 PGE2 NF-κB pathway Alzheimer’s disease
url	http://link.springer.com/article/10.1186/s40709-019-0102-1
work_keys_str_mv	AT lijiaogeng tanshinoneiiaattenuatesabinducedneurotoxicitybydownregulatingcox2expressionandpge2synthesisviainactivationofnfkbpathwayinshsy5ycells AT weiliu tanshinoneiiaattenuatesabinducedneurotoxicitybydownregulatingcox2expressionandpge2synthesisviainactivationofnfkbpathwayinshsy5ycells AT yongchen tanshinoneiiaattenuatesabinducedneurotoxicitybydownregulatingcox2expressionandpge2synthesisviainactivationofnfkbpathwayinshsy5ycells
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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

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