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 α (TNF-α), and nuclear factor κB (NF-κB) 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-α, NF-κB, 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.

在这项研究中，我们旨在显示5'-三磷酸腺苷（ATP）对舒尼替尼诱导的大鼠心脏损伤的影响。将大鼠（Ñ = 30）随机分为三组为舒尼替尼组（SG），舒尼替尼加ATP组（SAG），与健康对照组（HG）; SAG组腹膜内（ip）注射2 mg / kg ATP。与其他两组腹腔注射相同体积的生理盐水作为溶剂。1小时后，在SAG和SG组中，通过导管将25 mg / kg舒尼替尼口服到胃中。每天重复一次此过程，持续5周。在此期间结束时，处死所有动物并取出其心脏组织。丙二醛（MDA），总谷胱甘肽（tGSH），肿瘤坏死因子α（TNF- α）和核因子κB（NF- κ B）在大鼠心脏组织和肌钙蛋白I（TP-Ⅰ）大鼠的水平的血液样品进行了评价的水平。还在动物的心脏组织中进行了组织病理学分析。MDA，TNF- α，NF- κ B，和TP-I水平相比，SAG和HG组（分别为所述SG组高p <0.001）。SG组的tGSH水平低于SAG组和HG组（p<0.001）。对照组心肌纤维和血管的结构和形态正常。在SG组中，观察到明显的心肌组织损伤，肌纤维扩张，局部萎缩性肌纤维和血管充血。在SAG组中，观察到这些发现明显改善。我们首次证明了ATP的给药对舒尼替尼的心脏作用具有保护作用。