Evidence map›Paper›PMID 21449918›Full record

ArticleBritish journal of pharmacology2011

Kaempferol acts through mitogen-activated protein kinases and protein kinase B/AKT to elicit protection in a model of neuroinflammation in BV2 microglial cells.

S E Park, K Sapkota, S Kim, H Kim, S J Kim

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in British journal of pharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
95citing papers in PubMed, 3 pooled it
6.8field-weighted citation impact, top 3% 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

95 citing papers in PubMed, 3 syntheses or guidelines pooled it, 224 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
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  4. Trial
  5. Mechanistic convergence ofIBRO neuroscience reports · 2026
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  10. International journal of molecular sciences · 2026
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35 more citing papers are in PubMed but not listed here.

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

5 authors at 1 institution in 2 countries.

S E ParkDepartment of Biotechnology, Chosun University, Gwangju, Korea.
K Sapkota
S Kim
H Kim
S J Kim
Chosun University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposeKaempferol, a dietary flavonoid and phyto-oestrogen, is known to have anti-inflammatory properties. Microglial activation has been implicated in various neurodegenerative diseases. Anti-inflammatory effects of kaempferol and the underlying mechanisms were investigated by using LPS-stimulated microglial BV2 cells. EXPERIMENTAL APPROACH: Cell viability was measured using MTT and neutral red assays. elisa, Western blot, immunocytochemistry and electrophoretic mobility-shift assay were used to analyse NO, PGE(2) , TNF-α and IL-1β production, inducible NOS (iNOS), COX-2 expression and the involvement of signalling pathways such as toll-like receptor-4 (TLR4), MAPK cascades, PKB (AKT) and NF-κB. Accumulation of reaction oxygen species (ROS) was measured by nitroblue tetrazolium and 2'7'-dichlorofluorescein diacetate assay. Matrix metalloproteinase activity was investigated by zymography and immunoblot assay. Phagocytotic activity was assessed by use of latex beads. KEY

resultsKaempferol significantly attenuated LPS-induced NO, PGE(2) , TNF-α, IL-1β and ROS production and phagocytosis in a concentration-dependent manner. Kaempferol suppressed the expression of iNOS, COX-2, MMP-3 and blocked the TLR4 activation. Moreover, kaempferol inhibited LPS-induced NF-κB activation and p38 MAPK, JNK and AKT phosphorylation. CONCLUSION AND IMPLICATIONS: Kaempferol was able to reduce LPS-induced inflammatory mediators through the down-regulation of TLR4, NF-κB, p38 MAPK, JNK and AKT suggesting that kaempferol has therapeutic potential for the treatment of neuroinflammatory diseases.

Indexed as

AnimalsAnti-Inflammatory AgentsCells, CulturedCell SurvivalCyclooxygenase 2DinoprostoneInterleukin-1betaKaempferolsLipopolysaccharidesMatrix Metalloproteinase 3Matrix Metalloproteinase InhibitorsMiceMicrogliaMitogen-Activated Protein Kinase KinasesNF-kappa BNitric OxideAnti-Inflammatory AgentsCyclooxygenase 2DinoprostoneInterleukin-1betakaempferolKaempferolsLipopolysaccharidesMatrix Metalloproteinase 3Matrix Metalloproteinase InhibitorsMitogen-Activated Protein Kinase KinasesNF-kappa BNitric OxideNitric Oxide Synthase Type IINos2 protein, mousep38 Mitogen-Activated Protein KinasesProto-Oncogene Proteins c-aktPtgs2 protein, mouseReactive Oxygen SpeciesTlr4 protein, mouseToll-Like Receptor 4Tumor Necrosis Factor-alpha

Identifiers

PMID21449918
PMCPMC3195922
OpenAlexW1568243410

What OpenQuestion holds

Textmetadata
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.