Evidence map›Paper›PMID 24940388›Full record

ArticleExperimental and therapeutic medicine2014

Luteolin inhibits SH-SY5Y cell apoptosis through suppression of the nuclear transcription factor-κB, mitogen-activated protein kinase and protein kinase B pathways in lipopolysaccharide-stimulated cocultured BV2 cells.

Lihong Zhu, Wei Bi, Dan Lu, Chanjuan Zhang, Xiaoming Shu, Daxiang Lu

Open access · diamondAbstract read
In one paragraph

Article in Experimental and therapeutic medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

23 citing papers in PubMed, 54 citations in OpenAlex.

  1. Phytochemical and Anti-Ischemic Stroke Properties from theDrug design, development and therapy · 2026
    Review
  2. Review
  3. Therapeutic Expedition of Luteolin against Brain-related Disorders: An Updated Review.Combinatorial chemistry & high throughput screening · 2025
    Review
  4. Article
  5. Luteolin for neurodegenerative diseases: a review.Pharmacological reports : PR · 2024
    Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Luteolin Inhibits Fibrillary β-AmyloidMolecules (Basel, Switzerland) · 2017
    Article
  17. Article
  18. Review
  19. 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

6 authors at 2 institutions in 1 country.

Lihong ZhuDepartment of Pathophysiology, Institute of Brain Research, School of Medicine, Jinan University, Guangzhou, Guangdong 510632, P.R. China.
Wei BiDepartment of Neurology, First Affiliated Hospital of Jinan University, Guangzhou, Guangdong 510630, P.R. China.
Dan LuDepartment of Pathophysiology, Institute of Brain Research, School of Medicine, Jinan University, Guangzhou, Guangdong 510632, P.R. China.
Chanjuan ZhangDepartment of Pathophysiology, Institute of Brain Research, School of Medicine, Jinan University, Guangzhou, Guangdong 510632, P.R. China.
Xiaoming ShuDepartment of Pathophysiology, Institute of Brain Research, School of Medicine, Jinan University, Guangzhou, Guangdong 510632, P.R. China.
Daxiang LuDepartment of Pathophysiology, Institute of Brain Research, School of Medicine, Jinan University, Guangzhou, Guangdong 510632, P.R. China.
Jinan University · CNFirst Affiliated Hospital of Jinan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Microglial activation is one of the causative factors for neuroinflammation, which is associated with the pathophysiology of neurodegenerative diseases. Our previous study showed that the flavonoid luteolin inhibited several pro-inflammatory enzymes and pro-inflammatory cytokines that are induced by activated microglia; however, its effect on signaling pathways is currently unknown. The present study examined the effects of luteolin on signaling pathways stimulated by lipopolysaccharide (LPS), including Toll-like receptor-4 (TLR-4), nuclear transcription factor-κB (NF-κB), mitogen-activated protein kinase (MAPK) family and protein kinase B (Akt) pathways in murine microglial BV2 cells. In addition, BV2 microglia and SH-SY5Y neuroblastoma cells were cocultured to observe the indirect neuroprotective effects of luteolin. Luteolin inhibited the LPS-stimulated expression of TLR-4. In addition, luteolin blocked LPS-induced NF-κB, p38, JNK and Akt activation, but had no effect on ERK. When SH-SY5Y cells were cocultured with LPS-stimulated BV2 microglia, pretreatment with luteolin increased neuronal viability and reduced the number of apoptotic cells. These data suggest that luteolin has a beneficial effect on neuroinflammatory events in neurodegenerative diseases via suppression of the NF-κB, MAPK and Akt pathways in activated microglial cells.

Indexed as

luteolinmicrogliamitogen-activated protein kinaseneuroinflammationneuroprotectionnuclear transcription factor κBprotein kinase BToll-like receptor 4

Identifiers

PMID24940388
PMCPMC3991549
OpenAlexW2079858540

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.