Evidence map›Paper›PMID 26775664›Full record

ArticleActa pharmacologica Sinica2016

Sulforaphane prevents rat cardiomyocytes from hypoxia/reoxygenation injury in vitro via activating SIRT1 and subsequently inhibiting ER stress.

Yun-peng Li, Shu-lin Wang, Bei Liu, Lu Tang, Rong-ren Kuang, Xian-bao Wang, Cong Zhao, Xu-dong Song, Xue-ming Cao, Xiang Wu and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Acta pharmacologica Sinica, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

30 citing papers in PubMed, 51 citations in OpenAlex.

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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

13 authors at 3 institutions in 1 country.

Yun-peng LiDepartment of Cardiology, Zhujiang Hospital, Southern Medical University, Guangzhou 510280, China.
Shu-lin WangDepartment of Cardiology, Zhujiang Hospital, Southern Medical University, Guangzhou 510280, China.
Bei LiuDepartment of Cardiology, Zhujiang Hospital, Southern Medical University, Guangzhou 510280, China.
Lu TangDepartment of Cardiology, Zhujiang Hospital, Southern Medical University, Guangzhou 510280, China.
Rong-ren KuangDepartment of Cardiology, Zhujiang Hospital, Southern Medical University, Guangzhou 510280, China.
Xian-bao WangDepartment of Cardiology, Zhujiang Hospital, Southern Medical University, Guangzhou 510280, China.
Cong ZhaoDepartment of Cardiology, Zhujiang Hospital, Southern Medical University, Guangzhou 510280, China.
Xu-dong SongDepartment of Cardiology, Zhujiang Hospital, Southern Medical University, Guangzhou 510280, China.
Xue-ming CaoDepartment of Cardiology, He-nan Provincial People's Hospital, Zhengzhou 450003, China.
Xiang WuDepartment of Cardiology, Zhujiang Hospital, Southern Medical University, Guangzhou 510280, China.
Ping-zhen YangDepartment of Cardiology, Zhujiang Hospital, Southern Medical University, Guangzhou 510280, China.
Li-zi WangDepartment of Cardiology, Zhujiang Hospital, Southern Medical University, Guangzhou 510280, China.
Ai-hua ChenDepartment of Cardiology, Zhujiang Hospital, Southern Medical University, Guangzhou 510280, China.
Southern Medical University · CNZhujiang Hospital · CNHenan Provincial People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimSulforaphane (SFN), a natural dietary isothiocyanate, is found to exert beneficial effects for cardiovascular diseases. This study aimed to investigate the mechanisms underlying the protective effects of SFN in a model of myocardial hypoxia/reoxygenation (H/R) injury in vitro.

methodsCultured neonatal rat cardiomyocytes pretreated with SFN were subjected to 3-h hypoxia followed by 3-h reoxygenation. Cell viability and apoptosis were detected. Caspase-3 activity and mitochondrial membrane potential (ΔΨm) was measured. The expression of ER stress-related apoptotic proteins were analyzed with Western blot analyses. Silent information regulator 1 (SIRT1) activity was determined with SIRT1 deacetylase fluorometric assay kit.

resultsSFN (0.1-5 μmol/L) dose-dependently improved the viability of cardiomyocytes, diminished apoptotic cells and suppressed caspase-3 activity. Meanwhile, SFN significantly alleviated the damage of ΔΨm and decreased the expression of ER stress-related apoptosis proteins (GRP78, CHOP and caspase-12), elevating the expression of SIRT1 and Bcl-2/Bax ratio in the cardiomyocytes. Co-treatment of the cardiomyocytes with the SIRT1-specific inhibitor Ex-527 (1 μmol/L) blocked the SFN-induced cardioprotective effects.

conclusionSFN prevents cardiomyocytes from H/R injury in vitro most likely via activating SIRT1 pathway and subsequently inhibiting the ER stress-dependent apoptosis.

Indexed as

AnimalsApoptosisCardiotonic AgentsCell HypoxiaCells, CulturedCell SurvivalEndoplasmic Reticulum StressIsothiocyanatesMembrane Potential, MitochondrialMyocardial Reperfusion InjuryMyocytes, CardiacRatsRats, Sprague-DawleySignal TransductionSirtuin 1SulfoxidesCardiotonic AgentsIsothiocyanatesSirt1 protein, ratSirtuin 1sulforaphaneSulfoxides

Identifiers

PMID26775664
PMCPMC4775847
OpenAlexW2293684265

What OpenQuestion holds

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Registered trials

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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.