Levosimendan suppresses oxidative injury, apoptotic signaling and mitochondrial degeneration in streptozotocin-induced diabetic cardiomyopathy. (2nd January 2016)

• Record Type: Journal Article
• Authors: Akhtar, Md Sayeed; Pillai, Krishna Kolappa; Hassan, Quamrul; Ansari, Shahid Husain; Ali, Javed; Akhtar, Mohammed; Najmi, Abul Kalam
• Is Part Of: Clinical and experimental hypertension. Volume 38:Number 1(2016)
• Page Start: 10
• Page End: 22
• Publication Date: 2016-01-02
• Subjects: Cardiomyopathy -- diabetes -- levosimendan -- mitochondrial damage -- oxidative damage -- streptozotocin; Hypertension -- Chemotherapy -- Periodicals; Hypotensive agents -- Periodicals; 616.132
• DOI: 10.3109/10641963.2015.1047947
• Languages: English
• ISSNs: 1064-1963

Abstract

Abstract: Diabetic cardiomyopathy plays a major role in morbidity and mortality among cardiovascular disorder-related complications. This study was designed to explore long-term benefits of Levosimendan (LEVO) along with Ramipril and Insulin. Diabetic cardiomyopathy was induced using streptozotocin (STZ) at the dose of 25 mg/kg/body weight/day for three consecutive days in Wistar rats. Rats were randomly divided into 10 groups and treatments were started after 2 weeks of STZ administration. A gradual but severe hyperglycemia ( §§§ p < 0.001) was observed in all STZ-treated groups except those received insulin (2 U/day). LEVO alone and in combination with Ramipril and Insulin normalized (** p < 0.01) mean arterial pressure and heart rate, restored catalase, superoxide dismutase, malondialdehyde, glutathione level and also attenuated (*** p < 0.001) the raised serum levels of creatine kinase-heart type, lactate dehydrogenase, tumor necrosis factor-alpha, C-reactive protein, and caspase-3 level in heart tissue altered after STZ treatment. Myofibril degeneration, mitochondrial fibrosis and vacuolization occurred after STZ treatment, were also reversed by LEVO in combination with Ramipril and Insulin. The combination of LEVO with Ramipril and Insulin improved hemodynamic functions, maintained cardiac enzymes and ameliorated myofibril damage in diabetic cardiomyopathy.