Evidence map›Paper›PMID 29017559›Full record

ArticleLipids in health and disease2017

Salidroside protects against foam cell formation and apoptosis, possibly via the MAPK and AKT signaling pathways.

Jing Ni, Yuanmin Li, Weiming Li, Rong Guo

Open access · goldAbstract read
In one paragraph

Article in Lipids in health and disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

16 citing papers in PubMed, 35 citations in OpenAlex.

  1. Review
  2. Role ofCurrent medicinal chemistry · 2025
    Review
  3. Review
  4. Review
  5. Salidroside Reduced CaCell biochemistry and biophysics · 2024
    Article
  6. Review
  7. Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Protective Effects of Salidroside against Carbon Tetrachloride (CClInternational journal of molecular sciences · 2019
    Article
  13. Article
  14. Article
  15. Review
  16. 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

4 authors at 2 institutions in 1 country.

Jing NiDepartment of Cardiology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, 301 Yan Chang Zhong Road, Shanghai, 200072, China.
Yuanmin LiDepartment of Cardio-Thoracic Surgery, Shanghai Tenth People's Hospital, Tongji University School of Medicine, 301 Yan Chang Zhong Road, Shanghai, 200072, China.
Weiming LiDepartment of Cardiology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, 301 Yan Chang Zhong Road, Shanghai, 200072, China. lwmsoncentury@126.com.
Rong GuoDepartment of Cardiology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, 301 Yan Chang Zhong Road, Shanghai, 200072, China. doctorguorong@aliyun.com.
Shanghai Tenth People's Hospital · CNTongji University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundFoam cell formation and apoptosis are closely associated with atherosclerosis pathogenesis. We determined the effect of salidroside on oxidized low-density lipoprotein (ox-LDL)-induced foam cell formation and apoptosis in THP1 human acute monocytic leukemia cells and investigated the associated molecular mechanisms.

methodsTHP1-derived macrophages were incubated with salidroside for 5 h and then exposed to ox-LDL for 24 h to induce foam cell formation. Cytotoxicity, lipid deposition, apoptosis, and the expression of various proteins were tested using the CCK8 kit, Oil Red O staining, flow cytometry, and western blotting, respectively.

resultsOx-LDL treatment alone promoted macrophage-derived foam cell formation, while salidroside treatment alone inhibited it (p < 0.05). The number of early/late apoptotic cells decreased with salidroside treatment in a dose-dependent manner (p < 0.05). Salidroside dramatically upregulated nuclear factor erythroid 2-related factor 2, but had no effect on heme oxygenase-1 expression; moreover, it markedly downregulated ox-LDL receptor 1 and upregulated ATP-binding cassette transporter A1. Salidroside also obviously decreased the phosphorylation of JNK, ERK, p38 MAPK, and increased that of Akt. However, the total expression of these proteins was not affected.

conclusionBased on our findings, we speculate that salidroside can suppress ox-LDL-induced THP1-derived foam cell formation and apoptosis, partly by regulating the MAPK and Akt signaling pathways.

Indexed as

AntioxidantsApoptosisATP Binding Cassette Transporter, Subfamily G, Member 1Cell DifferentiationExtracellular Signal-Regulated MAP KinasesFoam CellsGene Expression RegulationGlucosidesHeme Oxygenase-1HumansLipoproteins, LDLMAP Kinase Kinase 4NF-E2-Related Factor 2Oxidation-ReductionOxidative Stressp38 Mitogen-Activated Protein KinasesAntioxidantsATP Binding Cassette Transporter, Subfamily G, Member 1Extracellular Signal-Regulated MAP KinasesGlucosidesHeme Oxygenase-1HMOX1 protein, humanLipoproteins, LDLMAP Kinase Kinase 4NFE2L2 protein, humanNF-E2-Related Factor 2oxidized low density lipoproteinp38 Mitogen-Activated Protein KinasesPhenolsProto-Oncogene Proteins c-aktrhodiolosideScavenger Receptors, Class EAkt pathwayFoam cellMAPK pathwaySalidrosideTHP1

Identifiers

PMID29017559
PMCPMC5635575
OpenAlexW2760856444

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.