Leptin protects cardiomyocytes from serum-deprivation-induced apoptosis by increasing anti-oxidant defence

摘要: 1. Leptin, an important adipose-derived hormone, can be associated with cardiac pathophysiology; however, the role of leptin in cardiomyocyte apoptosis is poorly understood. The present study examines serum-deprivation-induced primary cultured cardiomyocytes treated leptin. 2. Cardiomyocytes were subjected to serum deprivation presence or absence (5 50 nmol/L) for 48 h. Apoptosis was determined by Hoechst 33258 and Annexin V-FITC/propidium iodide dual staining. Cell viability, malondialdehyde (MDA) content, caspase 3 activation, expression enzyme activity superoxide dismutase (SOD) measured. Small interference RNA (siRNA) targeting SOD1 SOD2 used knockdown their measure apoptosis. 3. Serum caused nearly 30% cardiomyocytes, approximately 60% decrease cell viability. mRNA levels activated form greatly increased. In leptin, apoptotic rate reduced 15%, viability increased activation partially inhibited. Additionally, augmented lipid peroxidation (MDA formation) abolished, impaired activities restored SOD2, but not SOD1, stimulated Transfection siRNA that cause deficiency either attenuated anti-apoptotic effects 4. results suggest inhibits activating SOD. outlines direct actions disorders are related elevated levels.