Evidence map›Paper›PMID 30506291›Full record

ArticleNaunyn-Schmiedeberg's archives of pharmacology2019

Astaxanthin ameliorates cardiomyocyte apoptosis after coronary microembolization by inhibiting oxidative stress via Nrf2/HO-1 pathway in rats.

Yugang Xue, Chuang Sun, Qimeng Hao, Jin Cheng

RetractedAbstract readRetracted Publication
PubMed Publisher
In one paragraph

Article in Naunyn-Schmiedeberg's archives of pharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

19 citing papers in PubMed, 47 citations in OpenAlex.

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  10. Molecules (Basel, Switzerland) · 2021
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  11. Puerarin pretreatment attenuates cardiomyocyte apoptosis induced by coronary microembolization in rats by activating the PI3K/Akt/GSK-3β signaling pathway.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2021
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Yugang XueDepartment of Cardiology, Tangdu Hospital, Air Force Military Medical University, Xinsi Road, Xi'an, 710000, China.
Chuang SunDepartment of Cardiology, Tangdu Hospital, Air Force Military Medical University, Xinsi Road, Xi'an, 710000, China.
Qimeng HaoDepartment of Cardiology, Tangdu Hospital, Air Force Military Medical University, Xinsi Road, Xi'an, 710000, China.
Jin ChengDepartment of Cardiology, Tangdu Hospital, Air Force Military Medical University, Xinsi Road, Xi'an, 710000, China. JinCheng445@163.com.ORCID http://orcid.org/0000-0002-1708-4787
Tang Du Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Coronary microembolization (CME) caused by physical obstruction in coronary microcirculation induces myocardial apoptosis and cardiac dysfunction, and it was reported that the inactivation of the Nrf2/HO-1 signaling was involved in this process. Astaxanthin (AST) is a reddish pigment that belongs to keto-carotenoids. It is also a potent antioxidant and has been reported to activate Nrf2/HO-1 signaling in vein endothelial cells. However, it is still unknown whether AST is able to activate Nrf2/HO-1 signaling pathway to protect cardiac functions from CME in vivo. To address this question, rats were orally administrated with AST or AST plus Zinc protoporphyrin IX (ZnPP, a HO-1 inhibitor), followed by CME modeling operation. Then, cardiac function was evaluated by echocardiographic measurement. Myocardial infarction was measured by HBFP staining, and apoptosis was assessed by TUNEL staining. The protein levels and mRNA expressions of Bax and Bcl-2 were measured by Western blot and qRT-PCR, respectively. ELISA was performed to measure the activity of enzymes related to oxidative stress. AST pretreatment dramatically attenuated CME-induced cardiac dysfunction, myocardial infarction, and cardiomyocyte apoptosis. Mechanistically, AST suppressed CME-induced oxidative stress by re-activating Nrf2/HO-1 signaling. HO-1 inhibitor ZnPP completely eliminated the benefits of AST in CEM, supporting the critical role of Nrf2/HO-1 signaling in mediating the cardioprotective function of AST in CME. Conclusion: AST suppresses oxidative stress via activating Nrf2/HO-1 pathway and thus prevents CME-induced cardiomyocyte apoptosis and ameliorates cardiac dysfunction in rats.

Indexed as

AnimalsAntioxidantsApoptosisCoronary CirculationCoronary VesselsEmbolismHeme Oxygenase (Decyclizing)MicrocirculationMyocardial InfarctionMyocytes, CardiacNF-E2-Related Factor 2Oxidative StressRats, Sprague-DawleySignal TransductionXanthophyllsAntioxidantsastaxanthineHeme Oxygenase (Decyclizing)Hmox1 protein, ratNfe2l2 protein, ratNF-E2-Related Factor 2XanthophyllsAstaxanthinCardiomyocyte apoptosisCoronary microembolizationNrf2/HO-1 signalingOxidative stress

Identifiers

PMID30506291
OpenAlexW2903081842

What OpenQuestion holds

Textmetadata
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.