Evidence map›Paper›PMID 22658257›Full record

ArticleAtherosclerosis2012

Salvianolic acid B inhibits macrophage uptake of modified low density lipoprotein (mLDL) in a scavenger receptor CD36-dependent manner.

Yi Bao, Li Wang, Yanni Xu, Yuan Yang, Lifei Wang, Shuyi Si, Sunghee Cho, Bin Hong

Open access · greenAbstract read
In one paragraph

Article in Atherosclerosis, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed, 1 pooled it
11.3field-weighted citation impact, top 2% 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

44 citing papers in PubMed, 1 synthesis or guideline pooled it, 81 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Role of CD36 in central nervous system diseases.Neural regeneration research · 2024
    Review
  10. Review
  11. Cardiovascular & hematological agents in medicinal chemistry · 2023
    Article
  12. Article
  13. Article
  14. The role of CD36 in cardiovascular disease.Cardiovascular research · 2022
    Review
  15. Role of CD36 in cancer progression, stemness, and targeting.Frontiers in cell and developmental biology · 2022
    Review
  16. Article
  17. Review
  18. Review
  19. Review
  20. 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

8 authors at 2 institutions in 2 countries.

Yi BaoKey Laboratory of Biotechnology of Antibiotics of Ministry of Health, Institute of Medicinal Biotechnology, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.
Li Wang
Yanni Xu
Yuan Yang
Lifei Wang
Shuyi Si
Sunghee Cho
Bin Hong
Chinese Academy of Medical Sciences & Peking Union Medical College · CNBurke Medical Research Institute · US

Funding

The role of CD36 in ischemic inflammation and injuryR01HL082511 · NHLBI · WINIFRED MASTERSON BURKE MED RES INST · PI CHO, SUNGHEE · 2006 to 2014
$4.4M
NHLBI NIH HHS HL82511NHLBI NIH HHS R01 HL082511
6 · The paper itself

Abstract

CD36, a class B scavenger receptor, has been implicated in the pathogenesis of a host of vascular inflammatory diseases. Through a high-throughput screening (HTS) assay for CD36 antagonist, we previously identified salvianolic acid B (SAB), a hydrophilic component derived from the herb Danshen, as a potential candidate. Danshen, the dried roots of Salvia miltiorrhiza, has been widely used in China for the prevention and treatment of atherosclerosis-related disorders. Previous studies showed that SAB acted as an anti-oxidant by preventing lipid peroxidation and oxidized LDL (oxLDL) formation. The present study was to investigate the specificity and efficacy of SAB in the inhibition of CD36-mediated lipid uptake. SAB reduced modified LDL (mLDL) uptake in a dose-dependent manner in phorbol-12-myristate-13-acetate (PMA)-stimulated THP-1 and RAW 264.7 cells. In the CD36 silenced THP-1 cells, SAB had no effect in reducing mLDL uptake, whereas its overexpression in CHO cells reinstates the effect, indicating a specific involvement of SAB in antagonizing the CD36's function. Surface plasmon resonance (SPR) analysis revealed a direct binding of SAB to CD36 with a high affinity (K(D) = 3.74 μM), confirming physical interactions of SAB with the receptor. Additionally, SAB reduced oxLDL-induced CD36 gene expression in the cultured cell lines and primary macrophages. In ApoE KO mice fed a high fat diet, SAB reduced CD36 gene expression and lipid uptake in macrophages, showing its ability to antagonize CD36 pathways in vivo. These results demonstrate that SAB is an effective CD36 antagonist and suggest SAB as a potential anti-atherosclerotic agent.

Indexed as

AnimalsApolipoproteins EAtherosclerosisBenzofuransBiological TransportCD36 AntigensCell Line, TumorCHO CellsCricetinaeCricetulusDepsidesDisease Models, AnimalDose-Response Relationship, DrugHumansHyperlipidemiasHypolipidemic Agentsacetyl-LDLApolipoproteins EBenzofuransCD36 AntigensDepsidesHypolipidemic AgentsLipoproteins, LDLoxidized low density lipoproteinReceptors, LDLsalvianolic acid BTetradecanoylphorbol Acetate

Identifiers

PMID22658257
PMCPMC3389144
OpenAlexW2071357722

What OpenQuestion holds

Textmetadata
LicenceTDM
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.