Evidence map›Paper›PMID 36903379›Full record

ArticleMolecules (Basel, Switzerland)2023

Synthetic Glabridin Derivatives Inhibit LPS-Induced Inflammation via MAPKs and NF-κB Pathways in RAW264.7 Macrophages.

Jaejin Shin, Leo Sungwong Choi, Hyun Ju Jeon, Hyeong Min Lee, Sang Hyo Kim, Kwan-Woo Kim, Wonmin Ko, Hyuncheol Oh, Hyung Soon Park

Full text read
In one paragraph

Article in Molecules (Basel, Switzerland), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing 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

14 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Chemical profiling ofFrontiers in veterinary science · 2026
    Article
  5. Article
  6. A Narrative Review of the Multi-Target Mechanisms of Glabridin in Skin Lightening.Clinical, cosmetic and investigational dermatology · 2026
    Review
  7. 8-Methoxybicolosin C fromJournal of microbiology and biotechnology · 2025
    Article
  8. Article
  9. Review
  10. Article
  11. Subinhibitory concentrations of glabridin fromFrontiers in microbiology · 2024
    Article
  12. Article
  13. The Effects of 2International journal of molecular sciences · 2023
    Article
  14. 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

9 authors.

Jaejin ShinGlaceum Inc., Suwon 16675, Republic of Korea.ORCID 0000-0002-1879-6700
Leo Sungwong ChoiGlaceum Inc., Suwon 16675, Republic of Korea.ORCID 0000-0001-8850-0832
Hyun Ju JeonGlaceum Inc., Suwon 16675, Republic of Korea.
Hyeong Min LeeGlaceum Inc., Suwon 16675, Republic of Korea.ORCID 0000-0003-3065-6783
Sang Hyo KimGlaceum Inc., Suwon 16675, Republic of Korea.
Kwan-Woo KimDepartment of Herbal Crop Research, National Institute of Horticultural and Herbal Science, RDA, Eumseong 27709, Republic of Korea.
Wonmin KoDepartment of Marine Bio-Food Sciences, Chonnam National University, Yeosu 59626, Republic of Korea.
Hyuncheol OhCollege of Pharmacy, Wonkwang University, Iksan 54538, Republic of Korea.
Hyung Soon ParkGlaceum Inc., Suwon 16675, Republic of Korea.

Funding

Glaceum (South Korea) financial support
6 · The paper itself

Abstract

Glabridin is a polyphenolic compound with reported anti-inflammatory and anti-oxidative effects. In the previous study, we synthesized glabridin derivatives-HSG4112, (S)-HSG4112, and HGR4113-based on the structure-activity relationship study of glabridin to improve its biological efficacy and chemical stability. In the present study, we investigated the anti-inflammatory effects of the glabridin derivatives in lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages. We found that the synthetic glabridin derivatives significantly and dose-dependently suppressed the production of nitric oxide (NO) and prostaglandin E2 (PGE2), and decreased the level of inducible nitric oxygen synthase (iNOS) and cyclooxygenase-2 (COX-2) and the expression of pro-inflammatory cytokines interleukin-1β (IL-1β), IL-6, and tumor necrosis factor alpha (TNF-α). The synthetic glabridin derivatives inhibited the nuclear translocation of the NF-κB by inhibiting phosphorylation of the inhibitor of κB alpha (IκB-α), and distinctively inhibited the phosphorylation of ERK, JNK, and p38 MAPKs. In addition, the compounds increased the expression of antioxidant protein heme oxygenase (HO-1) by inducing nuclear translocation of nuclear factor erythroid 2-related factor 2 (Nrf2) through ERK and p38 MAPKs. Taken together, these results indicate that the synthetic glabridin derivatives exert strong anti-inflammatory effects in LPS-stimulated macrophages through MAPKs and NF-κB pathways, and support their development as potential therapeutics against inflammatory diseases.

Indexed as

LipopolysaccharidesNF-kappa BAnimalsAnti-Inflammatory AgentsCyclooxygenase 2InflammationIsoflavonesMacrophagesMiceNitric OxideNitric Oxide Synthase Type IIPhenolsRAW 264.7 CellsAnti-Inflammatory AgentsCyclooxygenase 2glabridinIsoflavonesLipopolysaccharidesNF-kappa BNitric OxideNitric Oxide Synthase Type IIPhenolsanti-inflammationglabridin derivativesHGR4113HSG4112 (vutiglabridin)LPS-stimulated macrophageNF-κB

Identifiers

PMID36903379
PMCPMC10004008

What OpenQuestion holds

Textfull text, public
LicenceCC BY
measurements read22
identifiers read2
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.