Department of Medical Analysis, Princess Aisha Bint Al-Hussein Faculty of Nursing and Health Sciences, Al-Hussein Bin Talal University, Jordan.
Department of Biology, Faculty of Science, Al-Hussein Bin Talal University, Jordan.
Life Sci. 2019 Mar 15;221:83-92. doi: 10.1016/j.lfs.2019.02.017. Epub 2019 Feb 8.
Hyperglycemia-mediated oxidative damage has been described as a major mechanism leading to pathologic changes associated with diabetic cardiomyopathy (DCM). Fisetin is a bioactive flavonol molecule found in many plants and possesses various biological activities. The present study investigated the protective effect of fisetin on diabetes-induced cardiac injury.
Diabetes was induced by streptozotocin (STZ) and both diabetic and control rats were treated with 2.5 mg/kg fisetin for six weeks.
Diabetic rats exhibited hyperglycemia, and increased glycosylated hemoglobin and serum lipids accompanied with significant hypoinsulinism. In addition, diabetic rats showed several histological alterations in the myocardium, and significantly increased serum troponin I, creatine kinase-MB and lactate dehydrogenase. Oxidative stress, inflammation and apoptosis markers were increased, whereas antioxidant defenses were significantly reduced in the diabetic heart. Treatment with fisetin alleviated hyperglycemia, hyperlipidemia and heart function markers, and minimized histological alterations in the myocardium. Fisetin suppressed oxidative stress, prevented inflammation and apoptosis, and boosted antioxidant defenses in the heart of diabetic rats.
Fisetin attenuated the development of DCM via amelioration of hyperglycemia/hyperlipidemia-mediated oxidative stress, inflammation and apoptosis. Therefore, it might be worth considering the therapeutic potential of fisetin for human DCM.
高血糖介导的氧化损伤被描述为导致与糖尿病心肌病（DCM）相关的病理变化的主要机制。非瑟酮是一种存在于许多植物中的生物活性类黄酮分子，具有多种生物学活性。本研究旨在探讨非瑟酮对糖尿病诱导的心脏损伤的保护作用。
链脲佐菌素（STZ）诱导糖尿病，糖尿病和对照组大鼠分别用 2.5mg/kg 非瑟酮治疗 6 周。
糖尿病大鼠表现为高血糖，糖化血红蛋白和血清脂质升高，同时伴有明显的胰岛素不足。此外，糖尿病大鼠的心肌出现多种组织学改变，血清肌钙蛋白 I、肌酸激酶-MB 和乳酸脱氢酶显著升高。氧化应激、炎症和细胞凋亡标志物增加，而糖尿病心脏中的抗氧化防御明显降低。非瑟酮治疗可减轻高血糖、高血脂和心脏功能标志物，最小化心肌的组织学改变。非瑟酮抑制氧化应激，预防炎症和细胞凋亡，并增强糖尿病大鼠心脏的抗氧化防御。
非瑟酮通过改善高血糖/高血脂介导的氧化应激、炎症和细胞凋亡来减轻 DCM 的发展。因此，非瑟酮可能值得考虑用于人类 DCM 的治疗潜力。
