17β-estradiol protects against doxorubicin-induced cardiotoxicity in male Sprague-Dawley rats by regulating NADPH oxidase and apoptosis genes

• DOI: 10.3892/mmr.2017.6332
• Publication Date: 2017-03-16T08:31:25Z
• Authors: Xiao-Juan Zhang; Xiao-Qing Cao; Chun-Sheng Zhang; Zhuo Zhao
• Keywords: Cardiotoxicity; Creatine kinase; Intraperitoneal injection

Doxorubicin (DOX) is one of the most effective chemotherapeutic agents for treatment a number malignancies. However, its use limited by serious cardiotoxic effects, which there are currently no reliable pharmacologic therapies. Estrogen has exhibited protective effects against cardiac stressors in male and female animal models; however, on DOX‑induced cardiotoxicity remain unknown. High mortality morbidity rates have been observed patients with cancer worldwide, DOX often administered to greater men than women. Therefore, present study employed Sprague-Dawley rats evaluate 17β-estradiol (E2) DOX-induced cardiotoxicity. A total 4 mg/kg was 14‑week‑old Sprague‑Dawley intraperitoneal injection twice week 2 weeks. At 3 weeks following first DOX, an echocardiographic revealed that administration significantly decreased ejection fraction fractional shortening 20 29%, respectively, when compared vehicle‑treated control (P<0.05). This associated heart weight, myofibrillar disorganization myofiber loss. The serum biomarkers injury, including alanine aminotransferase, aspartate lactate dehydrogenase creatine kinase, were increased vs. E2 daily subcutaneous body weight attenuated DOX. In addition, inhibited increase expression genes, nicotinamide adenine dinucleotide phosphate oxidase (NOX) 2, NOX4, B‑cell lymphoma 2‑associated X protein caspase 3. These results demonstrate may protect potentially through regulation NOX2, NOX4 apoptosis genes.