Evidence map›Paper›PMID 38849890›Full record

ArticleCell communication and signaling : CCS2024

Homotherapy for heteropathy: therapeutic effect of Butein in NLRP3-driven diseases.

Wenhao Liao, Yuchen Li, Jingwen Liu, Yu Mou, Mei Zhao, Juan Liu, Tianxin Zhang, Qin Sun, Jianyuan Tang, Zhilei Wang

Abstract read
In one paragraph

Article in Cell communication and signaling : CCS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
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

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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

4 citing papers in PubMed.

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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

10 authors.

Wenhao Liao *TCM Regulating Metabolic Diseases Key Laboratory of Sichuan Province, Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, 610075, China.
Yuchen Li *Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, 610075, China.
Jingwen Liu *Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, 610075, China.
Yu MouHospital of Chengdu University of Traditional Chinese Medicine, Chengdu, 610075, China.
Mei ZhaoSchool of Basic Medical Sciences, Chengdu University of Traditional Chinese Medicine, Chengdu, 610075, China.
Juan LiuTCM Regulating Metabolic Diseases Key Laboratory of Sichuan Province, Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, 610075, China.
Tianxin ZhangHospital of Chengdu University of Traditional Chinese Medicine, Chengdu, 610075, China.
Qin SunNational Traditional Chinese Medicine Clinical Research Base of the Affiliated Traditional Chinese Medicine, Hospital of Southwest Medical University, Luzhou, 646000, China.
Jianyuan TangTCM Regulating Metabolic Diseases Key Laboratory of Sichuan Province, Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, 610075, China. tangjy@cdutcm.edu.cn.
Zhilei WangTCM Regulating Metabolic Diseases Key Laboratory of Sichuan Province, Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, 610075, China. wangzl1993@outlook.com.

Funding

China Postdoctoral Science Foundation 2022MD723714National Natural Science Foundation of China 82204706Natural Science Foundation of Sichuan Province 24NSFSC6071Open Foundation of TCM Regulating Metabolic Diseases Key Laboratory of Sichuan Province SZKF202212
6 · The paper itself

Abstract

backgroundAberrant inflammatory responses drive the initiation and progression of various diseases, and hyperactivation of NLRP3 inflammasome is a key pathogenetic mechanism. Pharmacological inhibitors of NLRP3 represent a potential therapy for treating these diseases but are not yet clinically available. The natural product butein has excellent anti-inflammatory activity, but its potential mechanisms remain to be investigated. In this study, we aimed to evaluate the ability of butein to block NLRP3 inflammasome activation and the ameliorative effects of butein on NLRP3-driven diseases.

methodsLipopolysaccharide (LPS)-primed bone-marrow-derived macrophages were pretreated with butein and various inflammasome stimuli. Intracellular potassium levels, ASC oligomerization and reactive oxygen species production were also detected to evaluate the regulatory mechanisms of butein. Moreover, mouse models of LPS-induced peritonitis, dextran sodium sulfate-induced colitis, and high-fat diet-induced non-alcoholic steatohepatitis were used to test whether butein has protective effects on these NLRP3-driven diseases.

resultsButein blocks NLRP3 inflammasome activation in mouse macrophages by inhibiting ASC oligomerization, suppressing reactive oxygen species production, and upregulating the expression of the antioxidant pathway nuclear factor erythroid 2-related factor 2 (Nrf2). Importantly, in vivo experiments demonstrated that butein administration has a significant protective effect on the mouse models of LPS-induced peritonitis, dextran sodium sulfate-induced colitis, and high-fat diet-induced non-alcoholic steatohepatitis.

conclusionOur study illustrates the connotation of homotherapy for heteropathy, i.e., the application of butein to broaden therapeutic approaches and treat multiple inflammatory diseases driven by NLRP3.

Indexed as

ChalconesInflammasomesLipopolysaccharidesMacrophagesMice, Inbred C57BLNLR Family, Pyrin Domain-Containing 3 ProteinReactive Oxygen SpeciesAnimalsColitisDisease Models, AnimalMaleMiceNon-alcoholic Fatty Liver DiseasebuteinChalconesInflammasomesLipopolysaccharidesNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mouseReactive Oxygen SpeciesButeinColitisNLRP3 inflammasomeNon-alcoholic steatohepatitisNrf2Peritonitis

Identifiers

PMID38849890
PMCPMC11158000

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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.