We investigated the rosiglitazone (RSG) effect on adriamycin (ADM)‐induced cardio toxicity in experimental animals. Forty adult Wistar male rats were separated into four groups as follows: normal control; RSG (10 mg/kg)‐treated; ADM (10 mg/kg)‐administered; and ADM (10 mg/kg) + RSG (10 mg/kg)‐treated. Serum lipid level, different biochemical biomarkers, histological analysis, and nuclear factor erythroid 2‐related factor/heme oxygenase‐1 (Nrf2/HO‐1), Caspase 3, B‐cell lymphoma 2 (Bcl‐2), and Bax gene expression were assessed in serum and cardiac tissue samples. Our results show that RSG treatment in ADM‐administered animals significantly diminished low‐density lipoprotein cholesterol, triglyceride, and total cholesterol, and increases high‐density lipoprotein cholesterol (HDL‐c) in comparison with the ADM group. RSG treatment reduced the effect of ADM administration on cardiac dysfunction markers such as cardiac troponin T Creatine Kinase‐MB, aspartate aminotransferase, and lactate dehydrogenase, showing the amelioration of cardio toxicity in ADM‐administered rats. Additionally, RSG treatment significantly decreased the level of malondialdehyde and nitric oxide in cardiovascular tissue. RSG‐treated rats in combination with ADM likewise showed a significant increase in reduced glutathione, superoxide dismutase, catalase content, and the activity of glutathione peroxidase (GPx) as compared with ADM group. Moreover, RSG treatment in ADM rats significantly increased an Nrf2 and HO‐1 expression in comparison with ADM group. While in apoptosis parameters, RSG treatment in ADM rats significantly diminished a cleaved caspase‐3 and Bax expression as well as expanded Bcl‐2 expression when contrasted with ADM group of rats. In conclusion, RSG is capable of protecting heart toxicity in ADM‐treated animals through defensive effects on oxidative stress and biochemical markers.

中文翻译：

---

过氧化物酶体增殖剂γ激动剂罗格列酮通过抑制氧化应激和细胞凋亡对阿霉素诱导的心脏毒性的改善作用

我们在实验动物中研究了罗格列酮 (RSG) 对阿霉素 (ADM) 诱导的心脏毒性的影响。40 只成年 Wistar 雄性大鼠分为以下四组：正常对照组；RSG (10 mg/kg) 处理；ADM (10 mg/kg) 给药；和 ADM (10 mg/kg) + RSG (10 mg/kg) 处理。血清脂质水平、不同的生化生物标志物、组织学分析和核因子红细胞 2 相关因子/血红素加氧酶-1 (Nrf2/HO-1)、半胱天冬酶 3、B 细胞淋巴瘤 2 (Bcl-2) 和 Bax 基因表达在血清和心脏组织样本中进行了评估。我们的结果表明，与 ADM 组相比，ADM 给药组的 RSG 治疗显着降低了低密度脂蛋白胆固醇、甘油三酯和总胆固醇，并增加了高密度脂蛋白胆固醇 (HDL-c)。RSG 治疗降低了 ADM 给药对心脏功能障碍标志物的影响，如心肌肌钙蛋白 T 肌酸激酶-MB、天冬氨酸转氨酶和乳酸脱氢酶，表明 ADM 给药大鼠的心脏毒性有所改善。此外，RSG 治疗显着降低了心血管组织中丙二醛和一氧化氮的水平。与 ADM 组相比，RSG 治疗的大鼠与 ADM 组合同样显示出还原型谷胱甘肽、超氧化物歧化酶、过氧化氢酶含量和谷胱甘肽过氧化物酶 (GPx) 活性显着增加。此外，与 ADM 组相比，ADM 大鼠的 RSG 治疗显着增加了 Nrf2 和 HO-1 的表达。而在凋亡参数中，与 ADM 组大鼠相比，RSG 治疗 ADM 大鼠显着降低了裂解的 caspase-3 和 Bax 表达以及扩大的 Bcl-2 表达。总之，RSG 能够通过对氧化应激和生化标志物的防御作用来保护 ADM 治疗动物的心脏毒性。