Evidence map›Paper›PMID 37596540›Full record

ArticleBMC cardiovascular disorders2023

Allicin protects against LPS-induced cardiomyocyte injury by activating Nrf2-HO-1 and inhibiting NLRP3 pathways.

Fangyuan Sun, Kailiang Xu, Jiayi Zhou, Wei Zhang, Guihe Duan, Ming Lei

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BMC cardiovascular disorders, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

15 citing papers in PubMed, 15 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

6 authors at 3 institutions in 1 country.

Fangyuan Sun *Trauma emergency center, The Seventh People's Hospital of Shanghai University of Traditional Chinese Medicine, No.358, Datong Road, Pudong New Area, Shanghai, 200137, China.
Kailiang Xu *Department of Critical Care Medicine, The Seventh People's Hospital of Shanghai University of TCM, Shanghai, 200137, China.
Jiayi ZhouTrauma emergency center, The Seventh People's Hospital of Shanghai University of Traditional Chinese Medicine, No.358, Datong Road, Pudong New Area, Shanghai, 200137, China.
Wei ZhangTrauma emergency center, The Seventh People's Hospital of Shanghai University of Traditional Chinese Medicine, No.358, Datong Road, Pudong New Area, Shanghai, 200137, China.
Guihe DuanDepartment of Critical Care Medicine, The Shache County People's Hospital of Xinjiang Kashgar Prefecture, Xinjiang, 844710, China.
Ming LeiTrauma emergency center, The Seventh People's Hospital of Shanghai University of Traditional Chinese Medicine, No.358, Datong Road, Pudong New Area, Shanghai, 200137, China. leimsh@163.com.
Seventh People's Hospital of Shanghai · CNShanghai University of Traditional Chinese Medicine · CNPeople's Hospital of Xinjiang Uygur Autonomous Region · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAllicin is a bioactive compound with potent antioxidative activity and plays a protective effect in myocardial damage and fibrosis. The role and mechanism of Allicin in septic cardiomyopathy are unclear. In this study, we investigated the effects and underlying mechanisms of Allicin on lipopolysaccharide (LPS) induced injury in H9c2 cardiomyocytes.

methodsH9c2 cardiomyocyte cells were pretreated with Allicin (0, 25, 50, and 100 µM) for 2 h, followed by incubation with LPS (10 µg/mL) for 24 h at 37 °C. Cell viability (cell counting kit-8 [CCK-8]), apoptosis (TUNEL staining), oxidative stress (malondialdehyde [MDA] and superoxide dismutase [SOD]), and cytokines release (Interleukin beta [IL-β], Interleukin 6 [IL-6], and tumor necrosis factor-alpha [TNF-α]) were determined. The mRNA and protein expression of nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), and NLR family pyrin domain containing 3 (NLRP3) signaling pathway molecules were quantified by real-time quantitative PCR (RT-qPCR) and western blot, respectively.

resultsAllicin had no effect on H9c2 cell viability but attenuated LPS-induced injury, with increased cell viability, reduction in inflammatory cytokines release, apoptosis, reduced MDA, and increased SOD (P < 0.05). Additionally, Allicin increased Nrf2 and cellular HO-1 expressions in LPS-treated H9c2 cells. Moreover, Allicin modulated the NLRP3 inflammasome, increased the cleaved caspase-1 (p10) protein, and attenuated the LPS-induced increase in NLRP3, pro-IL-1β, and IL-1β proteins. Silencing of Nrf2 by siRNA (siNrf2) significantly attenuated Allicin-induced increase in cell viability and HO-1 and decrease in NLRP3 protein in LPS-stimulated H9c2 cells.

conclusionsAllicin protects cardiomyocytes against LPS‑induced injury through activation of Nrf2/HO-1 and inhibition of NLRP3 signaling pathways.

Indexed as

LipopolysaccharidesMyocytes, CardiacCytokinesDisulfidesHeme Oxygenase-1HumansInterleukin-6NF-E2-Related Factor 2NLR Family, Pyrin Domain-Containing 3 ProteinSulfinic AcidsallicinCytokinesDisulfidesHeme Oxygenase-1Interleukin-6LipopolysaccharidesNF-E2-Related Factor 2NLR Family, Pyrin Domain-Containing 3 ProteinSulfinic AcidsAllicinApoptosisCardiomyocytesInflammationLipopolysaccharideNLR family pyrin domain containing 3Nuclear factor erythroid 2-related factor 2

Identifiers

PMID37596540
PMCPMC10439633
OpenAlexW4385971377

What Socratic 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 Socratic graph.