The role of fetuin-A in vascular aging in the rat aorta


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BARIŞ Ö. , GACAR G. , YAZIR Y. , UTKAN T. , FINDIK O., KOMSUOĞLU ÇELİKYURT F. İ. , ...More

Turk J Vasc Surg, vol.31, no.1, pp.39-43, 2022 (Other Refereed National Journals)

  • Publication Type: Article / Article
  • Volume: 31 Issue: 1
  • Publication Date: 2022
  • Doi Number: 10.9739/tjvs.2022.1079
  • Title of Journal : Turk J Vasc Surg
  • Page Numbers: pp.39-43

Abstract

ABSTRACT
Objectives: In this study, we aimed to investigate the relationship between vascular system changes due to the increased inflammatory

response and oxidative stress with advanced age and fetuin-A levels in aortic tissues of a naturally aged rat model.

Materials and methods: A total of 16 Wistar albino rats were equally divided into two groups as the young group and the elderly group. The thoracic aorta was excised. The effect of aging on the aorta, proliferation, oxidative stress, and inflammation markers were evaluated using the real-time polymerase chain reaction method. Histological examination was performed to confirm the findings related to aging, and serum sampling was performed to determine fetuin-A levels.

Results: Interleukin-6 levels were lower in the elderly group (1.007 vs. 0.099-fold decrease, respectively; p=0.000). There was a moderate, positive correlation between fetuin-A and interleukin-6 levels (r=0.56; p=0.03). There was no significant difference in the antioxidant capacity as assessed by superoxide dismutase-1, while the oxidative stress markers were significantly higher in elderly rats (inducible nitric oxide synthase: 1 vs. 812.3-fold increase, respectively; p=0.006; endothelial nitric oxide synthase: 0.98 vs. 3.65-fold increase, respectively; p=0.001). There was a moderate, negative correlation between fetuin-A and endothelial nitric oxide synthase (r=-0.56; p=0.024).

Conclusion: Vascular senescence causes cell damage through inflammatory responses. Fetuin-A may indicate early vascular damage. Keywords: Atherosclerosis, fetuin-A, inflammation, rat, senescence.