Evidence map›Paper›PMID 25025067›Full record

ArticleBioMed research international2014

Amelioration of LPS-induced inflammation response in microglia by AMPK activation.

Chin-Chen Chen, Jiun-Tsai Lin, Yi-Fang Cheng, Cheng-Yi Kuo, Chun-Fang Huang, Shao-Hsuan Kao, Yao-Jen Liang, Ching-Yi Cheng, Han-Min Chen

Open access · hybridAbstract read
In one paragraph

Article in BioMed research international, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.6field-weighted citation impact, top 12% 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

28 citing papers in PubMed, 53 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. The Hallmarks of Ageing in Microglia.Cellular and molecular neurobiology · 2025
    Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Bamboo Shoot andCurrent issues in molecular biology · 2022
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Involvement of AMP-activated protein kinase in neuroinflammation and neurodegeneration in the adult and developing brain.International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience · 2019
    Review
  17. Article
  18. Adenine Inhibits the Growth of Colon Cancer Cells via AMP-Activated Protein Kinase Mediated Autophagy.Evidence-based complementary and alternative medicine : eCAM · 2019
    Article
  19. Anti-neuroinflammatory effects ofInternational journal of nanomedicine · 2019
    Article
  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

9 authors at 3 institutions in 1 country.

Chin-Chen ChenInstitute of Applied Science and Engineering, Catholic Fu-Jen University, New Taipei City 24205, Taiwan.
Jiun-Tsai LinEnergenesis Biomedical Co., Ltd., New Taipei City 24205, Taiwan.
Yi-Fang ChengEnergenesis Biomedical Co., Ltd., New Taipei City 24205, Taiwan.
Cheng-Yi KuoEnergenesis Biomedical Co., Ltd., New Taipei City 24205, Taiwan.
Chun-Fang HuangEnergenesis Biomedical Co., Ltd., New Taipei City 24205, Taiwan.
Shao-Hsuan KaoInstitute of Biochemistry and Biotechnology, Chung Shan Medical University, Taichung City 40201, Taiwan.
Yao-Jen LiangInstitute of Applied Science and Engineering, Catholic Fu-Jen University, New Taipei City 24205, Taiwan ; Department of Life Science, Catholic Fu-Jen University, New Taipei City 24205, Taiwan.
Ching-Yi ChengResearch Center for Industry of Human Ecology, Graduate Institute of Health Industry Technology, Department of Cosmetic Science, Chang Gung University of Science and Technology, Taoyuan 33303, Taiwan.
Han-Min ChenInstitute of Applied Science and Engineering, Catholic Fu-Jen University, New Taipei City 24205, Taiwan ; Energenesis Biomedical Co., Ltd., New Taipei City 24205, Taiwan ; Department of Life Science, Catholic Fu-Jen University, New Taipei City 24205, Taiwan.
Fu Jen Catholic University · TWChang Gung University of Science and Technology · TWChung Shan Medical University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Adenosine 5'-monophosphate-activated protein kinase (AMPK) is a key regulator of cellular energy homeostasis via modulating metabolism of glucose, lipid, and protein. In addition to energy modulation, AMPK has been demonstrated to associate with several important cellular events including inflammation. The results showed that ENERGI-F704 identified from bamboo shoot extract was nontoxic in concentrations up to 80 μM and dose-dependently induced phosphorylation of AMPK (Thr-172) in microglia BV2 cells. Our findings also showed that the treatment of BV2 with ENERGI-F704 ameliorated the LPS-induced elevation of IL-6 and TNF-α production. In addition, ENERGI-F704 reduced increased production of nitric oxide (NO) and prostaglandin E2 (PGE2) via downregulating the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX-2), respectively. Moreover, ENERGI-F704 decreased activated nuclear translocation and protein level of NF-κB. Inhibition of AMPK with compound C restored decreased NF-κB translocation by ENERGI-F704. In conclusion, ENERGI-F704 exerts inhibitory activity on LPS-induced inflammation through manipulating AMPK signaling and exhibits a potential therapeutic agent for neuroinflammatory disease.

Indexed as

AMP-Activated Protein KinasesCell LineDinoprostoneEnergy MetabolismHumansInflammationLipopolysaccharidesMicrogliaNitric OxidePlant ExtractsSasaTranscriptional ActivationAMP-Activated Protein KinasesDinoprostoneLipopolysaccharidesNitric OxidePlant Extracts

Identifiers

PMID25025067
PMCPMC4084681
OpenAlexW2082402551

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.