Evidence map›Paper›PMID 39052062›Full record

ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2024

Protective effects of nordalbergin against LPS-induced endotoxemia through inhibiting MAPK/NF-κB signaling pathway, NLRP3 inflammasome activation, and ROS production.

Pin-Rong Chen, Chia-Yang Li, Taha Yazal, I-Chen Chen, Po-Len Liu, Yi-Ting Chen, Ching-Chih Liu, Jung Lo, Tzu-Chieh Lin, Ching-Tang Chang and 6 more

Abstract read
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In one paragraph

Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

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

6 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
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  5. Review
  6. Review
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

16 authors.

Pin-Rong Chen *School of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, 80708, Taiwan.
Chia-Yang Li *Graduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, 80708, Taiwan.
Taha YazalSchool of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, 80708, Taiwan.
I-Chen ChenGraduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, 80708, Taiwan.
Po-Len LiuDepartment of Respiratory Therapy, College of Medicine, Kaohsiung Medical University, Kaohsiung, 80708, Taiwan.
Yi-Ting ChenDepartment of Pathology, Taichung Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Taichung, 427213, Taiwan.
Ching-Chih LiuGraduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, 80708, Taiwan.
Jung LoGraduate Institute of Clinical Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, 80708, Taiwan.
Tzu-Chieh LinGraduate Institute of Clinical Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, 80708, Taiwan.
Ching-Tang ChangGraduate Institute of Clinical Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, 80708, Taiwan.
Hsin-En WuGraduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, 80708, Taiwan.
Yuan-Ru ChenGraduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, 80708, Taiwan.
Wei-Chung ChengCancer Biology and Precision Therapeutics Center, China Medical University, Taichung, 40403, Taiwan.
Chien-Chih ChiuDepartment of Biotechnology, Kaohsiung Medical University, Kaohsiung, 80708, Taiwan.
Chi-Shuo ChenDepartment of Biomedical Engineering and Environmental Sciences, National Tsing Hua University, Hsinchu, 30013, Taiwan.
Shu-Chi WangDepartment of Medical Research, Kaohsiung Medical University Hospital, Kaohsiung, 80756, Taiwan. shuchiwang@kmu.edu.tw.

Funding

China Medical University Hospital DMR-112-056, DMR-113-190, and DMR-113-191China Medical University, Taiwan CMU111-IP-04 and CMU112-MF-25National Science and Technology Council, Taiwan, R.O.C. NSTC 111-2218-E-037-001, NSTC 111-2314-B-037-071-MY3, NSTC 112-2314-B-037-127, NSTC 112-2314-B-037-128, NSTC 112-2926-I-037-501-G, NSTC 112-2314-B-037-089, NSTC 112-2311-B-039 -001, NSTC 112-2622-E-039-001, NSTC 111-2622-E-039-004 and NSTC 112-2218-E-037-001NTHU-KMU Joint Research Project KT113P010
6 · The paper itself

Abstract

objectiveNordalbergin is a coumarin extracted from Dalbergia sissoo DC. To date, the biological effects of nordalbergin have not been well investigated. To investigate the anti-inflammatory responses and the anti-oxidant abilities of nordalbergin using lipopolysaccharide (LPS)-activated macrophages and LPS-induced sepsis mouse model. MATERIALS AND

methodsProduction of nitrite oxide (NO), prostaglandin E2 (PGE

resultsOur results indicated that nordalbergin reduced the production of NO and pro-inflammatory cytokines in vitro and ex vivo. Nordalbergin also suppressed iNOS and cyclooxygenase-2 expressions, decreased NF-κB activity, and attenuated MAPKs signaling pathway activation by decreasing JNK and p38 phosphorylation by LPS-activated J774A.1 macrophages. Notably, nordalbergin diminished NLRP3 inflammasome activation via repressing the maturation of IL-1β and caspase-1 and suppressing ROS production by LPS/ATP- and LPS/nigericin-activated J774A.1 macrophages. Furthermore, nordalbergin exhibited protective effects against the infiltration of inflammatory cells and also inhibited the levels of organ damage markers (AST, ALT, BUN) by LPS-challenged mice.

conclusionNordalbergin possesses anti-inflammatory effects in macrophage-mediated innate immune responses, alleviates ROS production, decreases NLRP3 activation, and exhibits protective effects against LPS-induced tissue damage in mice.

Indexed as

EndotoxemiaInflammasomesLipopolysaccharidesNF-kappa BNLR Family, Pyrin Domain-Containing 3 ProteinReactive Oxygen SpeciesAnimalsAnti-Inflammatory AgentsCell LineCoumarinsCytokinesMacrophagesMaleMAP Kinase Signaling SystemMiceMice, Inbred C57BLAnti-Inflammatory AgentsCoumarinsCytokinesInflammasomesLipopolysaccharidesNF-kappa BNitric OxideNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mouseReactive Oxygen Speciesanti-inflammationInnate immunityMacrophagesMAPKs/NF-κB/NLRP3 signaling pathwaysNordalbergin

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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.