The effects of pulsed magnetic field on the key elements responsible for synthesis and destruction of elastin-collagen in diabetic lung tissue

The effects of pulsed magnetic field on the key elements responsible for synthesis and destruction of elastin-collagen in diabetic lung tissue

Changes in the expression levels of genes responsible for synthesis-destruction of elastin-collagen and the occurrence of lung diseases are in correlation. Although, diabetes-related complications are important health problems, the mechanism by which diabetes exerts this effect is unclear. On the other hand, although the effect of pulsed magnetic field (PMF) in lung diseases has been shown, its mechanism of action is unknown. The study aimed to determine the effects of PMF on the key regulator elements of the synthesis-destruction of elastin-collagen at the transcriptional level. Rats were divided into groups as control, control + PMF 10Hz, diabetes, diabetes + PMF 10Hz. PMF groups were exposed to 10 Hz PMF for four weeks. In diabetic conditions, ELN, ELANE, and COL1A1 genes were dysregulated at the transcriptional level as their levels were 14.23±2.56; 7.62±1.37 and 0.24±0.04, respectively. Dysregulated ELN gene expressions were decreased to 6.17±1.97 by PMF application. There were no meaningful changes in gene expressions in control + PMF 10 Hz groups. The present study shows that ELN, ELANE, and COL1A1 may play a key role at the transcriptional level in the mechanism of diabetic-lung diseases. In addition, it may be said that “PMF shows its effect by re-regulating the expression level of ELN gene in diabetic lung tissues”. In future studies, ELN gene-targeted PMF application methods may be developed. Moreover, PMF application might not affect the genes that are responsible for elastin-collagen synthesis-destruction in healthy lungs when the PMF is applied on different tissues for the treatment of various diseases.

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Medicine Science-Cover
  • ISSN: 2147-0634
  • Yayın Aralığı: Yılda 4 Sayı
  • Başlangıç: 2012
  • Yayıncı: Effect Publishing Agency ( EPA )
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