NF-κB, TNF-α and IL-6 Levels in Liver and Kidney of High-Fructose-Fed Rats

Iskender, Hatice and Dokumacioglu, Eda and Saral, Sinan and Yenice, Guler and Sevim, Cigdem (2018) NF-κB, TNF-α and IL-6 Levels in Liver and Kidney of High-Fructose-Fed Rats. Journal of Advances in Medical and Pharmaceutical Sciences, 18 (3). pp. 1-7. ISSN 23941111

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Abstract

Background: Fructose constituting an important part of human diet, was reported to facilitate fat depositing in the abdominal region in case of excessive consumption, therefore increasing the risk of chronic illness more rapidly than expected, and inducing development of various diseases such as diabetes, metabolic syndrome, hypertension and atherosclerosis. The aim of this study was to investigate nuclear factor-kappa B (NF-κB), tumour necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) levels in liver and kidney tissues of high-fructose-fed rats and to determine the role of dietary addition of fructose on inflammation.

Methods: The rats were randomly divided into two groups of 7 rats as control (C) and fructose (F). The fructose group received 30% (v/w) fructose in drinking water for 8 weeks. Serum samples were used for aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), blood urea nitrogen (BUN) and uric acid measurements. The liver and kidney tissues of the rats were washed with 0.9% NaCl for TNF-α, IL-6 and NF-κB measurements.

Results: TNF-α, IL-6 and NF-κB levels in liver tissues were found significantly higher in the fructose group than the control group (p<0.001, p<0.05, p<0.001, respectively). TNF-α, IL-6 and NF-κB levels in the kidney tissue of the fructose group were statistically significantly higher than the control group (p<0.001, p<0.001, p<0.001, respectively).

Conclusion: Fructose fed diet increased liver and kidney damage through augmenting NF-κB, TNF-α and IL-6 levels.

Item Type: Article
Subjects: STM Library > Medical Science
Depositing User: Managing Editor
Date Deposited: 21 Apr 2023 05:01
Last Modified: 13 Jan 2024 04:17
URI: http://open.journal4submit.com/id/eprint/1829

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