Evidence map›Paper›PMID 33594608›Full record

ArticleIn vitro cellular & developmental biology. Animal2021

Dp44mT regulates the levels of inflammatory mediators through blocking NF-κB nuclear translocation in LPS-stimulated RAW 264.7 macrophages.

Jin-Ho Lim, Hee-Yun Kim, Jin Soo Lee, Hyung-Min Kim, Hyun-Ja Jeong

Open access · bronzeAbstract read
In one paragraph

Article in In vitro cellular & developmental biology. Animal, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.6field-weighted citation impact, top 34% 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

5 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Emerging Roles of the Iron Chelators in Inflammation.International journal of molecular sciences · 2022
    Review
  5. Article
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 2 institutions in 1 country.

Jin-Ho Lim *Department of Bio-Convergence System, Graduate School, Hoseo University, 20 Hoseo-ro,79 Beon-gil, Baebang-eup, Asan, 31499, Republic of Korea.
Hee-Yun Kim *Biochip Research Center, Hoseo University, 20, Hoseo-ro 79beon-gil, Baebang-eup, Asan, Chungnam, 31499, Republic of Korea.
Jin Soo LeeDepartment of Pharmacology, College of Korean Medicine, Kyung Hee University, Seoul, 130-701, Republic of Korea.
Hyung-Min KimDepartment of Pharmacology, College of Korean Medicine, Kyung Hee University, Seoul, 130-701, Republic of Korea.
Hyun-Ja JeongDepartment of Bio-Convergence System, Graduate School, Hoseo University, 20 Hoseo-ro,79 Beon-gil, Baebang-eup, Asan, 31499, Republic of Korea. hjjeong@hoseo.edu.
Kyung Hee University · KRHoseo University · KR

Funding

Ministry of Education 2018R1D1A1B07042113
6 · The paper itself

Abstract

Inflammation is increased by infection with pathogens such as viruses, bacteria, and parasites. High levels of inflammatory mediators and infiltration of macrophages into inflammatory lesions were reported in severe inflammatory diseases. Here, the aim of this study was to evaluate an anti-inflammatory activity of di-2-pyridylketone-4,4-dimethyl-3-thiosemicarbazone (Dp44mT) on lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages. Dp44mT (1-100 ng/mL) had no effect on viability of RAW 264.7 macrophages. Dp44mT (100 ng/mL) significantly reduced LPS-induced release of nitric oxide and expression of inducible nitric oxide synthase and cyclooxygenase-2. A significant upregulation of tumor necrosis factor (TNF)-α and interleukin (IL)-6 by LPS stimulation was downregulated by treatment with Dp44mT. Dp44mT blocked activation of nuclear factor-κB by the interruption of IκBα phosphorylation. Dp44mT suppressed the phagocytosis. Furthermore, administration of Dp44mT significantly reduced the serum levels of TNF-α and IL-6 in LPS-treated mice without side effects. In conclusion, these results indicate that Dp44mT has an anti-inflammatory activity and may be of therapeutic significant for the prevention and treatment of inflammatory diseases.

Indexed as

AnimalsCell NucleusCell SurvivalCyclooxygenase 2Inflammation MediatorsInterleukin-6LipopolysaccharidesMacrophagesMaleMiceMice, Inbred C57BLNF-kappa BNitric OxideNitric Oxide Synthase Type IIPhagocytosisProtein TransportCyclooxygenase 2di-2-pyridylketone-4,4-dimethyl-3-thiosemicarbazoneInflammation MediatorsInterleukin-6LipopolysaccharidesNF-kappa BNitric OxideNitric Oxide Synthase Type IIRNA, MessengerThiosemicarbazonesTumor Necrosis Factor-alphaCyclooxygenase-2Dp44MtInflammatory cytokineNitric oxideNuclear factor-κB

Identifiers

PMID33594608
PMCPMC7886191
OpenAlexW3131864801

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.