The 35th ESVS Hybrid Annual Meeting, Rotterdam, Netherlands, Rotterdam, Netherlands, 28 - 29 September 2021, pp.1
Background: Fetuin-A is a prevalent anti-inflammatory glycoprotein that resists proinflammatory cytokine production. Low fetuin-A levels indicate an increased risk for cardiovascular diseases. As fetuin-A levels decrease, the production of inflammatory cytokines increases as a result of adipocyte-related inflammation. With this study, the natural aged rat model that we created for two years, we aimed to predict fetuin-A in the natural senescence process with vascular especially aortic aging and possible affected inflammation markers.
Methods: Sixteen Wistar albino rats were equally divided into two groups as the young group and the elderly group. The thoracic aorta was excised for analysis. The effect of aging on the aorta, proliferation, oxidative stress and inflammation markers were evaluated by Real Time Polymerase Chain Reaction method. Histological evaluation was performed to confirm the findings related to aging, and serum sampling was performed to determine fetuin-A levels.
Results: Interleukin-6 levels which are an inflammatory markers were also lower in elderly group (1,007 versus 0,099; p=0,000 ) and there was a correlation between fetuin-A and interleukin-6 levels (r: 0,56; p=0,03). While there was no significant difference of antioxidant capacity assessed by superoxide dismutase-1, the oxidative stress markers were significantly higher in elderly rats than young’s ( Inducible nitric oxide synthase: 1 vs. 812,3, p=0,006; endothelial nitric oxide synthase: 0,98 vs. 3,65, p=0,001). There was a 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: Senescence, fetuin-A, rat, inflammation, atherosclerosis.