Evidence map›Paper›PMID 26295477›Full record

ArticlePloS one2015

Brazilin Limits Inflammatory Responses through Induction of Prosurvival Autophagy in Rheumatoid Fibroblast-Like Synoviocytes.

Hyunji Lee, Seong Wook Kang, Hee Sun Byun, Juhee Jeon, Kyeong Ah Park, Kidong Kang, Wonhyoung Seo, Minho Won, Jeong Ho Seok, Man-Deuk Han and 2 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
3.1field-weighted citation impact, top 10% 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

12 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Article
  3. Brazilin alleviates acute lung injury via inhibition of ferroptosis through the SIRT3/GPX4 pathway.Apoptosis : an international journal on programmed cell death · 2025
    Article
  4. Unlocking the therapeutic mechanism ofFrontiers in pharmacology · 2024
    Review
  5. Review
  6. Review
  7. Review
  8. The Role of Autophagy and Mitophagy in Bone Metabolic Disorders.International journal of biological sciences · 2020
    Review
  9. Article
  10. Article
  11. Article
  12. 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

12 authors at 3 institutions in 2 countries.

Hyunji LeeDepartment of Pharmacology, College of Medicine, Chungnam National University, Daejeon, Republic of Korea; Division of Rheumatology, Department of Internal Medicine, College of Medicine, Chungnam National University, Daejeon, Republic of Korea.
Seong Wook KangDivision of Rheumatology, Department of Internal Medicine, College of Medicine, Chungnam National University, Daejeon, Republic of Korea.
Hee Sun ByunDepartment of Pharmacology, College of Medicine, Chungnam National University, Daejeon, Republic of Korea.
Juhee JeonDepartment of Pharmacology, College of Medicine, Chungnam National University, Daejeon, Republic of Korea.
Kyeong Ah ParkDepartment of Pharmacology, College of Medicine, Chungnam National University, Daejeon, Republic of Korea.
Kidong KangDepartment of Pharmacology, College of Medicine, Chungnam National University, Daejeon, Republic of Korea.
Wonhyoung SeoDepartment of Pharmacology, College of Medicine, Chungnam National University, Daejeon, Republic of Korea.
Minho WonDepartment of Pharmacology, College of Medicine, Chungnam National University, Daejeon, Republic of Korea.
Jeong Ho SeokDepartment of Pharmacology, College of Medicine, Chungnam National University, Daejeon, Republic of Korea.
Man-Deuk HanDepartment of Biology, Soonchunhyang University, Asan, Chungnam, Republic of Korea.
Han-Ming ShenDepartment of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.
Gang Min HurDepartment of Pharmacology, College of Medicine, Chungnam National University, Daejeon, Republic of Korea.
Chungnam National University · KRNational University of Singapore · SGSoonchunhyang University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Brazilin is an active compound of Caesalpinia sappan L. (Leguminosae), which possesses pro-apoptotic and anti-inflammation potentials depending on the specific cell type. However, it is largely unknown whether autophagy is implicated in the mechanism underlying its chemotherapeutic and anti-inflammatory effects in rheumatoid arthritis (RA). Here, we show that treatment of RA fibroblast-like synoviocytes (FLS) with brazilin results in enhanced level of autophagic flux, evidenced by accumulation of autophagosome and increased level of lipidated LC3 (LC3-II), which is mainly mediated by enhanced production of reactive oxygen species (ROS). Interestingly, long-term exposure of brazilin was able to restore cell survival against the cytotoxity, exclusively in RA FLS, but not in normal fibroblast. Importantly, such a restoration from brazilin-induced cytotoxity in RA FLS was completely abrogated after co-treatment with autophagy inhibitors including NH4Cl or chloroquine. Furthermore, we found that the pretreatment of RA FLS with brazilin reduced LPS- or TNF-induced NF-κB activation and the secretion of inflammatory cytokines in parallel with the enhanced autophagic flux. Such anti-NF-κB potentials of brazilin were drastically masked in RA FLS when autophagy was suppressed. These results suggest that brazilin is capable of activating autophagy exclusively in RA FLS, and such inducible autophagy promotes cell survival and limits inflammatory response.

Indexed as

AnimalsAnti-Inflammatory AgentsArthritis, RheumatoidAutophagyBenzopyransCaesalpiniaCells, CulturedFibroblastsHumansMiceNF-kappa BNIH 3T3 CellsReactive Oxygen SpeciesSynovial MembraneAnti-Inflammatory AgentsBenzopyransbrazilinNF-kappa BReactive Oxygen Species

Identifiers

PMID26295477
PMCPMC4546660
OpenAlexW1846341045

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.