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Article: Sodium tanshinone IIA sulfonate protects against Aβ‐induced cell toxicity through regulating Aβ process

TitleSodium tanshinone IIA sulfonate protects against Aβ‐induced cell toxicity through regulating Aβ process
Authors
Keywords
Aβ degration
Aβ generation
Sodium tanshinone IIA sulfonate
Issue Date2020
PublisherWiley Open Access for Foundation for Cellular and Molecular Medicine. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=1582-1838
Citation
Journal of Cellular and Molecular Medicine, 2020, v. 24 n. 6, p. 3328-3335 How to Cite?
AbstractSodium tanshinone IIA sulfonate (STS) has been reported to prevent Alzheimer's disease (AD). However, the mechanism is still unknown. In this study, two in vitro models, Aβ‐treated SH‐SY5Y cells and SH‐SY5Y human neuroblastoma cells transfected with APPsw (SH‐SY5Y‐APPsw cells), were employed to investigate the neuroprotective of STS. The results revealed that pretreatment with STS (1, 10 and 100 µmol/L) for 24 hours could protect against Aβ (10 µmol/L)‐induced cell toxicity in a dose‐dependent manner in the SH‐SY5Y cells. Sodium tanshinone IIA sulfonate decreased the concentrations of reactive oxygen species, malondialdehyde, NO and iNOS, while increased the activities of superoxide dismutase and glutathione peroxidase in the SH‐SY5Y cells. Sodium tanshinone IIA sulfonate decreased the levels of inflammatory factors (IL‐1β, IL‐6 and TNF‐α) in the SH‐SY5Y cells. In addition, Western blot results revealed that the expressions of neprilysin and insulin‐degrading enzyme were up‐regulated in the SH‐SY5Y cells after STS treatment. Furthermore, ELISA and Western blot results showed that STS could decrease the levels of Aβ. ELISA and qPCR results indicated that STS could increase α‐secretase (ADAM10) activity and decrease β‐secretase (BACE1) activity. In conclusion, STS could protect against Aβ‐induced cell damage by modulating Aβ degration and generation. Sodium tanshinone IIA sulfonate could be a promising candidate for AD treatment.
Persistent Identifierhttp://hdl.handle.net/10722/288529
ISSN
2019 Impact Factor: 4.486
2015 SCImago Journal Rankings: 1.941
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorZhang, DP-
dc.contributor.authorLu, XY-
dc.contributor.authorHe, SC-
dc.contributor.authorLi, WY-
dc.contributor.authorAo, R-
dc.contributor.authorLeung, FCY-
dc.contributor.authorZhang, ZM-
dc.contributor.authorChen, QB-
dc.contributor.authorZhang, SJ-
dc.date.accessioned2020-10-07T01:50:14Z-
dc.date.available2020-10-07T01:50:14Z-
dc.date.issued2020-
dc.identifier.citationJournal of Cellular and Molecular Medicine, 2020, v. 24 n. 6, p. 3328-3335-
dc.identifier.issn1582-1838-
dc.identifier.urihttp://hdl.handle.net/10722/288529-
dc.description.abstractSodium tanshinone IIA sulfonate (STS) has been reported to prevent Alzheimer's disease (AD). However, the mechanism is still unknown. In this study, two in vitro models, Aβ‐treated SH‐SY5Y cells and SH‐SY5Y human neuroblastoma cells transfected with APPsw (SH‐SY5Y‐APPsw cells), were employed to investigate the neuroprotective of STS. The results revealed that pretreatment with STS (1, 10 and 100 µmol/L) for 24 hours could protect against Aβ (10 µmol/L)‐induced cell toxicity in a dose‐dependent manner in the SH‐SY5Y cells. Sodium tanshinone IIA sulfonate decreased the concentrations of reactive oxygen species, malondialdehyde, NO and iNOS, while increased the activities of superoxide dismutase and glutathione peroxidase in the SH‐SY5Y cells. Sodium tanshinone IIA sulfonate decreased the levels of inflammatory factors (IL‐1β, IL‐6 and TNF‐α) in the SH‐SY5Y cells. In addition, Western blot results revealed that the expressions of neprilysin and insulin‐degrading enzyme were up‐regulated in the SH‐SY5Y cells after STS treatment. Furthermore, ELISA and Western blot results showed that STS could decrease the levels of Aβ. ELISA and qPCR results indicated that STS could increase α‐secretase (ADAM10) activity and decrease β‐secretase (BACE1) activity. In conclusion, STS could protect against Aβ‐induced cell damage by modulating Aβ degration and generation. Sodium tanshinone IIA sulfonate could be a promising candidate for AD treatment.-
dc.languageeng-
dc.publisherWiley Open Access for Foundation for Cellular and Molecular Medicine. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=1582-1838-
dc.relation.ispartofJournal of Cellular and Molecular Medicine-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.subject-
dc.subjectAβ degration-
dc.subjectAβ generation-
dc.subjectSodium tanshinone IIA sulfonate-
dc.titleSodium tanshinone IIA sulfonate protects against Aβ‐induced cell toxicity through regulating Aβ process-
dc.typeArticle-
dc.identifier.emailLeung, FCY: feonalcy@hku.hk-
dc.identifier.authorityLeung, FCY=rp02269-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1111/jcmm.15006-
dc.identifier.pmid31989795-
dc.identifier.pmcidPMC7131914-
dc.identifier.scopuseid_2-s2.0-85078674264-
dc.identifier.hkuros314759-
dc.identifier.volume24-
dc.identifier.issue6-
dc.identifier.spage3328-
dc.identifier.epage3335-
dc.identifier.isiWOS:000509469400001-
dc.publisher.placeUnited Kingdom-

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