Adenosine analogs and electromagnetic fields inhibit prostaglandin E2 release in bovine synovial fibroblasts.

Osteoarthritis and cartilage · 2009 · Benefit · Low evidence

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BenefitLow evidencePaper 4983

TNF-alpha and LPS increased PGE2 release in bovine synovial fibroblasts. Exposure to EMFs (75 Hz, 1.5 mT) for 24 h inhibited PGE2 production without adenosine agonists and enhanced the inhibitory effects of CHA, CGS 21680, and NECA; the EMF inhibitory effect …

Study snapshot

PublicationOsteoarthritis and cartilage · 2009
Study typein_vitro
Reported directionBenefit
Evidence ratingLow

Abstract

OBJECTIVE: To investigate the role of adenosine analogs and electromagnetic field (EMF) stimulation on prostaglandin E(2) (PGE(2)) release and cyclooxygenase-2 (COX-2) expression in bovine synovial fibroblasts (SFs). METHODS: SFs isolated from synovia were cultured in monolayer. Saturation and binding experiments were performed by using typical adenosine agonists: N6-cyclohexyladenosine (CHA, A(1)), 2-[p-(2-carboxyethyl)-phenetyl-amino]-5'-N-ethylcarboxamidoadenosine (CGS 21680, A(2A)), 5'-N-ethylcarboxamidoadenosine (NECA, non-selective), N6-(3-iodobenzyl)2-chloroadenosine-5'-N-methyluronamide (Cl-IB-MECA, A(3)). SFs were treated with TNF-alpha (10 ng/ml) and lipopolysaccharide (LPS) (1 microg/ml) to activate inflammatory response. Adenosine analogs were added to control and TNF-alpha- or LPS-treated cultures both in the absence and in the presence of adenosine deaminase (ADA) which is used to deplete endogenous adenosine. Parallel cultures were exposed to EMFs (75 Hz, 1.5 mT) during the period in culture (24h). PGE(2) release was measured by immunoassay. COX-2 expression was evaluated by RT-PCR. RESULTS: TNF-alpha and LPS stimulated PGE(2) release. All adenosine agonists, except for Cl-IB-MECA, significantly inhibited PGE(2) production. EMFs inhibited PGE(2) production in the absence of adenosine agonists and increased the effects of CHA, CGS 21680 and NECA. In ADA, the inhibition on PGE(2) release induced by CHA, CGS and NECA was stronger than in the absence of ADA and the EMF-inhibitory effect was lost. Changes in PGE(2) levels were associated to modification of COX-2 expression. CONCLUSIONS: This study supports anti-inflammatory activities of A(1) and A(2A) adenosine receptors and EMFs in bovine SFs. EMF activity appears mediated by an EMF-induced up-regulation of A(2A) receptors. Biophysical and/or pharmacological modulation of adenosine pathways may play an important role to control joint inflammation.

Machine Enhanced Logic

AI evidence extraction

Structured fields below were generated from the paper’s abstract and metadata to make the evidence easier to inspect. Automated extraction may be incomplete or incorrect; verify important details against the original paper.

Study typein_vitro
Effect directionbenefit
PopulationBovine synovial fibroblasts (SFs) cultured in monolayer
Sample sizeNot supplied
ExposureELF · 7.5e-05 MHz · 24h
Evidence strengthLowConfidence: 78% · Peer reviewed: yes

Main findings

TNF-alpha and LPS increased PGE2 release in bovine synovial fibroblasts. Exposure to EMFs (75 Hz, 1.5 mT) for 24 h inhibited PGE2 production without adenosine agonists and enhanced the inhibitory effects of CHA, CGS 21680, and NECA; the EMF inhibitory effect was lost in the presence of adenosine deaminase. Changes in PGE2 were associated with modifications in COX-2 expression.

Outcomes measured

  • Prostaglandin E2 (PGE2) release
  • Cyclooxygenase-2 (COX-2) expression
  • Adenosine receptor agonist effects (A1, A2A, non-selective, A3) on inflammatory response

Limitations

  • In vitro study in bovine synovial fibroblasts; findings may not generalize to humans or in vivo conditions
  • Sample size not reported in abstract
  • Exposure conditions limited to a single frequency (75 Hz), flux density (1.5 mT), and duration (24 h)
View raw extracted JSON
{
  "study_type": "in_vitro",
  "exposure": {
    "band": "ELF",
    "source": "other",
    "frequency_mhz": 7.5e-05,
    "sar_wkg": null,
    "duration": "24h"
  },
  "population": "Bovine synovial fibroblasts (SFs) cultured in monolayer",
  "sample_size": null,
  "outcomes": [
    "Prostaglandin E2 (PGE2) release",
    "Cyclooxygenase-2 (COX-2) expression",
    "Adenosine receptor agonist effects (A1, A2A, non-selective, A3) on inflammatory response"
  ],
  "main_findings": "TNF-alpha and LPS increased PGE2 release in bovine synovial fibroblasts. Exposure to EMFs (75 Hz, 1.5 mT) for 24 h inhibited PGE2 production without adenosine agonists and enhanced the inhibitory effects of CHA, CGS 21680, and NECA; the EMF inhibitory effect was lost in the presence of adenosine deaminase. Changes in PGE2 were associated with modifications in COX-2 expression.",
  "effect_direction": "benefit",
  "limitations": [
    "In vitro study in bovine synovial fibroblasts; findings may not generalize to humans or in vivo conditions",
    "Sample size not reported in abstract",
    "Exposure conditions limited to a single frequency (75 Hz), flux density (1.5 mT), and duration (24 h)"
  ],
  "evidence_strength": "low",
  "confidence": 0.78,
  "peer_reviewed_likely": "yes",
  "keywords": [
    "electromagnetic fields",
    "ELF-EMF",
    "75 Hz",
    "1.5 mT",
    "bovine synovial fibroblasts",
    "prostaglandin E2",
    "PGE2",
    "COX-2",
    "adenosine receptors",
    "A1",
    "A2A",
    "TNF-alpha",
    "LPS",
    "inflammation"
  ],
  "suggested_hubs": []
}
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AI-extracted fields are generated from the abstract and metadata and may be incomplete or incorrect. This material is for informational purposes and is not medical advice.

Identifiers and source

DOI: 10.1016/j.joca.2008.06.002
PubMed: 18640059

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