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The therapeutic nuclear magnetic resonance changes the balance in intracellular calcium and reduces the interleukin-1β induced increase of NF-κB activity in chondrocytes


1, 2, 3, 4, 5

 

  1. Ludwig Boltzmann Department for Rehabilitation, Ludwig Boltzmann Cluster for Arthritis and Rehabilitation, Saalfelden, Austria. lbi.groebming@aon.at
  2. Ludwig Boltzmann Department for Rehabilitation, Ludwig Boltzmann Cluster for Arthritis and Rehabilitation, Saalfelden, Austria.
  3. Department of Special Anaesthesia and Pain Therapy, Medical University of Vienna, Austria.
  4. Department of Special Anaesthesia and Pain Therapy, Medical University of Vienna, Austria.
  5. Department of Special Anaesthesia and Pain Therapy, Medical University of Vienna, Austria.

CER10520
2018 Vol.36, N°2
PI 0294, PF 0301
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PMID: 29185963 [PubMed]

Received: 20/04/2017
Accepted : 01/08/2017
In Press: 28/11/2017
Published: 18/04/2018

Abstract

OBJECTIVES:
Osteoarthritis as the main chronic joint disease is characterised by the destruction of articular cartilage. Developing new, more effective and in particular non-invasive methods to achieve pain reduction of OA patients are of exceptional interest. Clinical observations demonstrated positive effects of therapeutically applied low nuclear magnetic resonance (NMRT) for the treatment of painful disorders of the musculoskeletal system. In this study the cellular mechanism of action of NMRT was examined on chondrocytes.
METHODS:
Cal-78 human chondrosarcoma cells were kept under inflammatory conditions by application of IL-1β. NMRT treated cells were tested for changes in histamine induced Ca2+ release by fura-2 calcium imaging. The effects of IL-1β and of NMRT treatment were further tested by determining intracellular ATP concentrations and the activity of MAP-kinases and NF-κB.
RESULTS:
NMRT influenced the intracellular calcium signalling by elevating the basal [Ca2+]i. The peak calcium concentration evoked by 10 μM histamine was increased by IL-1β and this increase was reversed under NMRT treatment. Screening of different kinase-activities revealed an apparent increase in activity of MAPK/ERK and MAPK/JNK in NMRT stimulated cells, p38 was downregulated. The IL-1β-induced decline in intracellular ATP and the elevated NF-κB activity was reversed under NMRT stimulation.
CONCLUSIONS:
Under inflammatory conditions, NMRT influenced cellular functions by modulating cellular calcium influx and/or calcium release. Further, NMRT induced changes in MAPK activities such as down-regulation of NF-κB and increasing intracellular ATP might help to stabilise chondrocytes and delay cartilage damage due to OA.

Rheumatology Article