2026-10-18T23:56:58Zhttps://ebyu-rdlopen.rawdatalibrary.net/oai/request

oai:ebyu-rdlopen.rawdatalibrary.net:ebyu/183482026-10-18T20:56:31Zopenairedrivercom_ebyu_10000col_ebyu_10001

Investigation of Changes in Apoptosis and Adipokine Biomarkers in Rats With Experimental HypothyroidismÇOBAN, T. AbdulkadirUSLU, HamitUSLU, Gözde ATİLABardas, EbruBiyolojiKalp ve Kalp Damar SistemiKimyaİnorganik ve NükleerObjective: In this study, it was aimed to investigate the changes in apoptosis and adipokine biomarkers in rats with propylthio uracil (PTU)-induced hypothyroidism. Methods: This study was carried out on 14 Sprague–Dawley male rats. While 10 mg/kg PTU was given intraperitoneally to the hypothyroid group for 15 days, physiological saline was also applied to the control group. At the end of the study, heart and serum samples were taken from the sacrificed animals. Thyroid stimulating hormone, fT4, irisin, adiponectin, BCL2, and TP53 levels were determined in these samples by enzyme-linked immunosorbent assay. Results: Although body weights increased in both groups on day 15 of the study, this increase was significant only in the hypothyroid group (P = .002). The body weights of the hypo thyroid group on the 15th day were higher than the control group (P = .048). Serum thyroid-stimulating hormone levels of the hypothyroid group (P = .000) were higher than the control group, and fT4 levels (P = .000) were lower. It was observed that irisin levels increased in hypothyroidism (P = .000), but ADP levels did not change. In addition, it was determined that BCL2 level, one of the important antiapoptotic markers, decreased in the hypothyroid group (P = .039), whereas the proapoptotic TP53 level increased, but this increase was not statistically significant. Conclusion: It suggests that the increase in irisin levels deter mined in the heart tissue may be due to cardiac hypertrophy induced by hypothyroidism and that abnormal changes in the levels of thyroid hormones may induce apoptosis via the intrin sic pathway by reducing the level of antiapoptotic signaling pro teins such as BCL2 by disrupting cell metabolism and cycle.2022Articlehttps://rdlopen.rawdatalibrary.net/r/ebyu/18348https://doi.org/10.54614/abcr.2021.210242687-4520enArchives of Basic and Clinical Researchinfo:eu-repo/semantics/openAccessinfo:eu-repo/semantics/articlehttps://ebyu-rdlopen.rawdatalibrary.net/tr/items/ebyu/18348