Evidence map›Paper›PMID 23341883›Full record

ArticlePloS one2013

TanshinoneIIA and cryptotanshinone protect against hypoxia-induced mitochondrial apoptosis in H9c2 cells.

Hyou-Ju Jin, Xiao-Liang Xie, Ji-Ming Ye, Chun-Guang Li

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
21.7field-weighted citation impact, top 1% 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

24 citing papers in PubMed, 74 citations in OpenAlex.

  1. Review
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  9. L-type CaScience signaling · 2020
    Article
  10. HMGB1 decreases CCR-2 expression and migration of M2 macrophages under hypoxia.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2019
    Article
  11. Review
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  14. Review
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  19. Cryptotanshinone inhibits TNF-α-induced LOX-1 expression by suppressing reactive oxygen species (ROS) formation in endothelial cells.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2016
    Article
  20. Article
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

4 authors at 3 institutions in 2 countries.

Hyou-Ju JinTraditional & Complementary Medicine Program, RMIT Health Innovations Research Institute, School of Health Sciences, RMIT University, Bundoora, Victoria, Australia.
Xiao-Liang Xie
Ji-Ming Ye
Chun-Guang Li
RMIT University · AUHebei Academy of Agriculture and Forestry Sciences · CNWestern Sydney University · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondrial apoptosis pathway is an important target of cardioprotective signalling. Tanshinones, a group of major bioactive compounds isolated from Salvia miltiorrhiza, have been reported with actions against inflammation, oxidative stress, and myocardial ischemia reperfusion injury. However, the actions of these compounds on the chronic hypoxia-related mitochondrial apoptosis pathway have not been investigated. In this study, we examined the effects and molecular mechanisms of two major tanshonones, tanshinone IIA (TIIA) and cryptotanshinone (CT) on hypoxia induced apoptosis in H9c2 cells. Cultured H9c2 cells were treated with TIIA and CT (0.3 and 3 μΜ) 2 hr before and during an 8 hr hypoxic period. Chronic hypoxia caused a significant increase in hypoxia inducible factor 1α expression and the cell late apoptosis rate, which was accompanied with an increase in caspase 3 activity, cytochrome c release, mitochondria membrane potential and expression of pro-apoptosis proteins (Bax and Bak). TIIA and CT (0.3 and 3 μΜ), in concentrations without affecting the cell viability, significantly inhibited the late apoptosis and the changes of caspase 3 activity, cytochrome c release, and mitochondria membrane potential induced by chronic hypoxia. These compounds also suppressed the overexpression of Bax and reduced the ratio of Bax/Bcl-2. The results indicate that TIIA and CT protect against chronic hypoxia induced cell apoptosis by regulating the mitochondrial apoptosis signaling pathway, involving inhibitions of mitochondria hyperpolarization, cytochrome c release and caspase 3 activity, and balancing anti- and pro-apoptotic proteins in Bcl-2 family proteins.

Indexed as

AbietanesAnimalsApoptosisCaspase 3Caspase InhibitorsCell HypoxiaCell SurvivalCyclosporineCytochromes cCytoprotectionEnzyme ActivationHypoxia-Inducible Factor 1, alpha SubunitMembrane Potential, MitochondrialMitochondriaMyocytes, CardiacPhenanthrenesAbietanesCaspase 3Caspase InhibitorscryptotanshinoneCyclosporineCytochromes cHypoxia-Inducible Factor 1, alpha SubunitPhenanthrenesProto-Oncogene Proteins c-bcl-2tanshinone

Identifiers

PMID23341883
PMCPMC3544838
OpenAlexW2029038340

What OpenQuestion holds

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LicenceCC BY
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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.