Evidence map›Paper›PMID 30927050›Full record

ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2019

α-Mangostin suppresses NLRP3 inflammasome activation via promoting autophagy in LPS-stimulated murine macrophages and protects against CLP-induced sepsis in mice.

Yun Ge, Xin Xu, Qiqiang Liang, Yongshan Xu, Man Huang

Abstract read
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In one paragraph

Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.9field-weighted citation impact, top 13% 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

21 citing papers in PubMed, 39 citations in OpenAlex.

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  11. The Interplay Between Autophagy and Regulated Necrosis.Antioxidants & redox signaling · 2023
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  15. Frontiers in cellular and infection microbiology · 2021
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  16. Review
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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

5 authors at 1 institution in 1 country.

Yun GeDepartment of General Intensive Care Unit, The Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, 310052, China.
Xin XuDepartment of General Intensive Care Unit, The Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, 310052, China.
Qiqiang LiangDepartment of General Intensive Care Unit, The Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, 310052, China.
Yongshan XuDepartment of General Intensive Care Unit, The Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, 310052, China.
Man HuangDepartment of General Intensive Care Unit, The Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, 310052, China. 20130505@zju.edu.cn.ORCID http://orcid.org/0000-0002-3777-1437
Second Affiliated Hospital of Zhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe major mechanism of sepsis is immunosuppression caused by host response dysfunction. It has been found that α-Mangostin (α-M) is a potential candidate as a treatment for multiple inflammatory and immune disorders. To date, the role of α-M in host response during sepsis remains unexplored. METHODS AND

resultsHerein, we examined the effect of α-M on macrophages-mediated host response in the presence of lipopolysaccharide (LPS), and the vital organ function, inflammatory response, and survival rate in septic mice. In murine peritoneal macrophages, α-M induced autophagy and then inhibited LPS-stimulated NLRP3 inflammasome activation, as well as interleukin-1β (IL-1β) production. Moreover, α-M improved phagocytosis and killing of macrophages, and increased M2 macrophages numbers after LPS stimulation. Furthermore, in vivo experiment suggested that α-M reduced serum levels of tumor necrosis factor-α (TNF-α), interferon-γ (IFN-γ), IL-1β, alanine transaminase (ALT), aspartate transaminase (AST), and creatinine (Cr), whilst increased that of interleukin-10 (IL-10) in caecal ligation and puncture (CLP) mice.

conclusionTaken together, these findings showed that α-M-mediated macrophages autophagy contributed to NLRP3 inflammasome inactivation and α-M exerted organ protection in septic mice.

Indexed as

AnimalsAutophagyCells, CulturedCytokinesLipopolysaccharidesMacrophages, PeritonealMaleMice, Inbred BALB CNLR Family, Pyrin Domain-Containing 3 ProteinSepsisXanthonesCytokinesLipopolysaccharidesmangostinNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mouseXanthonesAutophagyMacrophagesNLRP3 inflammasomeSepsisα-Mangostin

Identifiers

PMID30927050
OpenAlexW2926359842

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.