Browsing by Author "Kara, A., V"

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The Effect of Adenosine Triphosphate on Sunitinib-Induced Cardiac Injury in Rats
(Sage Publications Ltd, 2020) Aldemir, M. N.; Simsek, M.; Kara, A., V; Ozcicek, F.; Mammadov, R.; Yazici, G. N.; Suleyman, H.
In this study, we aimed to show the effect of adenosine 5 '-triphosphate (ATP) on sunitinib-induced cardiac injury in rats. The rats (n = 30) were divided equally into three groups as sunitinib group (SG), sunitinib plus ATP group (SAG), and healthy group (HG); 2 mg/kg ATP was injected intraperitoneally (ip) to the SAG group. Same volume normal saline as solvent was administered ip to the other two groups. After 1 h, 25 mg/kg sunitinib was applied orally via catheter to stomach in the SAG and SG groups. This procedure was repeated once daily for 5 weeks. At the end of this period, all animals were sacrificed and their cardiac tissue was removed. Malondialdehyde (MDA), total glutathione (tGSH), tumor necrosis factor alpha (TNF-alpha), and nuclear factor kappa B (NF-kappa B) levels in rats' cardiac tissues and troponin I (Tp-I) levels in rats' blood samples were evaluated. Histopathological analysis was also performed in cardiac tissues of the animals. MDA, TNF-alpha, NF-kappa B, and Tp-I levels were higher in the SG group compared to the SAG and HG groups (p < 0.001). tGSH levels of the SG group were lower than the SAG and HG groups (p < 0.001). The structure and morphology of cardiac muscle fibers and blood vessels were normal in the control group. In the SG group, obvious cardiac muscle tissue damage with dilated myofibers, locally atrophic myofibers, and congested blood vessels were observed. In the SAG group, marked amelioration in these findings was observed. We showed this for the first time that ATP administration exerts a protective effect against cardiac effects of sunitinib.
Effect of Taxifolin on Doxorubicin-Induced Oxidative Cardiac Damage in Rats: a Biochemical and Histopathological Evaluation
(Pakistan Agricultural Scientists Forum, 2024) Aldemir, M. N.; Kara, A., V; Mammadov, R.; Yazici, G. N.; Cicek, B.; Yavuzer, B.; Suleyman, H.
Doxorubicin is a widely used anthracycline-derived broad-spectrum antitumoral antibiotic drug. However, cardiotoxicity due to doxorubicin treatment has warranted dose reduction or complete discontinuation in certain cases. The role of oxidative stress in the pathogenesis of doxorubicin-induced cardiotoxicity has been previously demonstrated. Against this background, this study aimed to investigate the protective effect of the potent antioxidant flavone taxifolin against possible oxidative heart damage biochemically and histopathologically induced by doxorubicin. Albino Wistar male rats were divided into three groups: healthy controls (HG), a group given doxorubicin alone (DG), and a group given taxifolin + doxorubicin ( TDG). Taxifolin was administered orally at a dose of 50 mg/kg via gavage. Doxorubicin was injected intraperitoneally at a dose of 5 mg/kg. This procedure was repeated for 7 days. The results of the biochemical experiment showed that taxifolin significantly inhibited doxorubicin-induced malondialdehyde increases and glutathione decreases in heart tissues. In addition, taxifolin significantly suppressed the increases in cardiac damage markers, such as serum troponin I, creatine kinase, and creatine kinase-MB, induced by doxorubicin. Taxifolin treatment has also been histopathologically shown to alleviate doxorubicin-induced heart tissue damage. Accordingly, the results of the present study suggest that taxifolin may be useful in the treatment of doxorubicin-induced oxidative heart damage.