Pulsed magnetic field maintains vascular homeostasis against H2O2-induced oxidative stress.


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Günay İ., Baldan İ., Tokuş M., Coşkun Ç., Öcal I., Çiçek F.

General physiology and biophysics, cilt.39, sa.6, ss.579-586, 2020 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 39 Sayı: 6
  • Basım Tarihi: 2020
  • Doi Numarası: 10.4149/gpb_2020035
  • Dergi Adı: General physiology and biophysics
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, BIOSIS, EMBASE, MEDLINE
  • Sayfa Sayıları: ss.579-586
  • Çukurova Üniversitesi Adresli: Evet

Özet

Pulsed magnetic fields (PMFs) have significant therapeutic effects on many disorders. However, the effects of PMF on vascular homeostasis remain unclear. Therefore, in the present study, we investigated the role of in vivo PMF in maintaining vascular homeostasis during H2O2-induced oxidative stress. For this purpose, rats were exposed to PMF (40 Hz, 1.5 mT) for 1 h for a period of 30 days, following which their thoracic aortas were excised. H2O2 was exogenously applied to the aortic rings. Constrictions were measured in a tissue bath using an electrophysiological technique. Bcl-2 and endothelial nitric oxide synthase (eNOS) protein levels were determined by Western blotting. We found lesser H2O2-induced vasoconstriction in the PMF group than in the control group in endothelium-intact (E+) rings. As H2O2 also induces apoptosis, after incubation with H2O2 (40 min) to induce early apoptosis, we added KCl and measured KCl-induced contractions. All the groups, endothelium intact or denuded (E-) showed decreased responses; however, we still observed the effect of PMF in the E+ group due to increased endothelial activity. In addition, PMF increased the expression of the eNOS protein, which might be a key target of PMF. Our results suggest that in vivo application of PMF protects vascular responses through endothelium-mediated mechanisms during oxidative stress. Therefore, PMF might play a protective role against vascular diseases.