Evidence map›Paper›PMID 31989795›Full record

ArticleJournal of cellular and molecular medicine2020

Sodium tanshinone IIA sulfonate protects against Aβ-induced cell toxicity through regulating Aβ process.

Da-Peng Zhang, Xin-Yi Lu, Si-Chen He, Wan-Yan Li, Ran Ao, Feona Chung-Yin Leung, Zhi-Min Zhang, Qu-Bo Chen, Shi-Jie Zhang

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 22% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

10 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.

  1. Pooled it
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 4 institutions in 2 countries.

Da-Peng ZhangThe First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.ORCID 0000-0001-6962-0433
Xin-Yi LuBiological Resource Center, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, China.
Si-Chen HeDepartment of Neurology, The People's Hospital of Baiyun District Guangzhou, Guangzhou, China.
Wan-Yan LiThe First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Ran AoThe First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Feona Chung-Yin LeungLKS Faculty of Medicine, School of Chinese Medicine, The University of Hong Kong, Pokfulam, Hong Kong, China.
Zhi-Min ZhangThe First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Qu-Bo ChenBiological Resource Center, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, China.
Shi-Jie ZhangDepartment of Neurology, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, China.ORCID 0000-0001-5399-7260
First Affiliated Hospital of Guangzhou Medical University · CNGuangzhou University of Chinese Medicine · CNChinese University of Hong Kong · HKPeople's Hospital of Shiyan · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sodium 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.

Indexed as

ADAM10 ProteinAlzheimer DiseaseAmyloid beta-PeptidesAmyloid Precursor Protein SecretasesAspartic Acid EndopeptidasesCell Line, TumorCell SurvivalCytokinesGlutathione PeroxidaseHumansInsulysinMalondialdehydeMembrane ProteinsNeprilysinNeuroprotective AgentsNitric OxideADAM10 ProteinADAM10 protein, humanAmyloid beta-PeptidesAmyloid Precursor Protein SecretasesAspartic Acid EndopeptidasesBACE1 protein, humanCytokinesGlutathione PeroxidaseInsulysinMalondialdehydeMembrane ProteinsNeprilysinNeuroprotective AgentsNitric OxideNitric Oxide Synthase Type IINOS2 protein, humanPhenanthrenesReactive Oxygen SpeciesSuperoxide Dismutasetanshinone II A sodium sulfonateAβAβ degrationAβ generationsodium tanshinone IIA sulfonate

Identifiers

PMID31989795
PMCPMC7131914
OpenAlexW3003191975

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.