Evidence map›Paper›PMID 37622701›Full record

ArticleCurrent pharmaceutical biotechnology2024

5-methylthiopentyl Isothiocyanate, a Sulforaphane Analogue, Inhibits Pro-inflammatory Cytokines by Regulating LPS/ATP-mediated NLRP3 Inflammasome Activation.

Su-Bin Choi, Ji-Hye Kim, Sehee Kwon, Na-Hyun Ahn, Joo-Hee Lee, Woong-Suk Yang, Cheorl-Ho Kim, Seung-Hoon Yang

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Article in Current pharmaceutical biotechnology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.2field-weighted citation impact, top 41% 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

1 citing paper in PubMed, 1 citations in OpenAlex.

  1. Immunomodulatory Effects and Regulatory Mechanisms of (Journal of agricultural and food chemistry · 2024
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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

8 authors at 3 institutions in 1 country.

Su-Bin ChoiDepartment of Biomedical Engineering, College of Life Science and Biotechnology, Dongguk University, Seoul, 04620, Republic of Korea.
Ji-Hye KimDepartment of Biomedical Engineering, College of Life Science and Biotechnology, Dongguk University, Seoul, 04620, Republic of Korea.
Sehee KwonDepartment of Biomedical Engineering, College of Life Science and Biotechnology, Dongguk University, Seoul, 04620, Republic of Korea.
Na-Hyun AhnDepartment of Biomedical Engineering, College of Life Science and Biotechnology, Dongguk University, Seoul, 04620, Republic of Korea.
Joo-Hee LeeDepartment of Biomedical Engineering, College of Life Science and Biotechnology, Dongguk University, Seoul, 04620, Republic of Korea.
Woong-Suk YangNational Institute for Nanomaterials Technology (NINT), POSTECH, 77, Pohang, 37673, Republic of Korea.
Cheorl-Ho KimDepartment of Biological Sciences, Sungkyunkwan University and Samsung Advanced Institute of Health Science and Technology, Suwon, 1649, Republic of Korea.
Seung-Hoon YangDepartment of Biomedical Engineering, College of Life Science and Biotechnology, Dongguk University, Seoul, 04620, Republic of Korea.ORCID 0000-0002-6880-8861
Dongguk University · KRPohang University of Science and Technology · KRSamsung (South Korea) · KR

Funding

Basic Science Research Program Grant nos. NRF- 2015R1A6A3A04058568, NRF-2020R1F1A1076240, and NRF-2021R1C1C1009743)Ministry of Health & Welfare and Ministry of Science and ICT, Republic of Korea Grant No.: HU21C0161
6 · The paper itself

Abstract

backgroundPro-inflammatory cytokines secreted from activated macrophages and astrocytes are crucial mediators of inflammation for host defense. Among them, the secretion of IL-1β, a major pro-inflammatory cytokine, is especially mediated by the activation of NLRP3 inflammasome. Pro-IL-1β, which is produced in response to the invaded pathogens, such as LPS, is cleaved and matured in the NLRP3 inflammasome by the recognition of ATP. Excessively activated IL-1β induces other immune cells, resulting in the up-regulation of inflammation. Therefore, regulation of NLRP3 inflammasome can be a good strategy for alleviating inflammation.

objectiveOur study aimed to examine whether 5-methylthiopentyl isothiocyanate, a sulforaphane analogue (berteroin), has an anti-inflammatory effect on the NLRP3 inflammasome activation induced by LPS and ATP.

methodsPrimary bone marrow-derived macrophages (BMDMs) and astrocytes were stimulated by LPS and ATP with the treatment of 5-methylthiopentyl isothiocyanate, a sulforaphane analogue. The secretion of pro-inflammatory cytokines was measured by ELISA, and the expression level of NLRP3 inflammasome-associated proteins was detected by western blot. The association of NLRP3 inflammasome was assessed by co-immunoprecipitation, and the formation of ASC specks was evaluated by fluorescent microscope.

results5-methylthiopentyl isothiocyanate, a sulforaphane analogue (berteroin), decreased the release of pro-inflammatory cytokines, IL-1β, and IL-6 in the BMDMs. Berteroin notably prevented the formation of both NLRP3 inflammasome and ASC specks, which reduced the secretion of IL-1β. Additionally, berteroin reduced the IL-1β secretion and cleaved IL-1β expression in the primary astrocytes. DISCUSSION AND

conclusionThese results indicated the anti-inflammatory effects of 5- methylthiopentyl isothiocyanate (berteroin) by regulating NLRP3 inflammasome activation, suggesting that berteroin could be the potential natural drug candidate for the regulation of inflammation.

Indexed as

Adenosine TriphosphateAnti-Inflammatory AgentsCytokinesInflammasomesIsothiocyanatesLipopolysaccharidesMacrophagesMice, Inbred C57BLNLR Family, Pyrin Domain-Containing 3 ProteinAnimalsAstrocytesCells, CulturedInterleukin-1betaMiceSulfoxidesAdenosine TriphosphateAnti-Inflammatory AgentsCytokinesInflammasomesInterleukin-1betaIsothiocyanatesLipopolysaccharidesNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mousesulforaphaneSulfoxides5-methylthiopentyl isothiocyanateASC speck.astrocytea sulforaphane analogue (berteroin)inflammationNLRP3 inflammasomeprimary bone marrow-derived macrophages (BMDMs)pro-inflammatory cytokine

Identifiers

PMID37622701
OpenAlexW4386152411

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.