Cardio protective hypolipidemic activity of amino guanidine against Streptozotocin induced diabetic mice heart (an In vivo) and high glucose induced lipid accumulation cardiac fibroblasts (an in vitro study)

Abstract

This study mainly will focus on cardio protective antilipidemic activity of Aminguanidine against streptozotocin induced diabetic heart and high glucose induced lipid synthesis in H9C2 cardiac myoblasts. Excess lipid accumulation is one of the most diabetes associated complications in diabetic patients. Excess lipid may be stored as triglycerides, but are also shunted into non-oxidative pathways that disrupt normal cellular signaling leading to organ dysfunction and in some cases apoptosis, a process termed lipotoxicity. Lipid accumulation in cardiac turns Obesity and insulin resistance are associated with ectopic lipid deposition in multiple tissues including heart. Single dose of Streptozotocin (100 mg/kg) were given tail vein for diabetic induction. Normal and diabetic mice receive Aminoguanidine orally (100mg/kg) throughout the study period of eight weeks. H9C2 cardiac myoblasts grown and exposed to high glucose and Aminoguanidine for 48 hrs to study whether Aminoguanidine can successfully reduces high glucose induced lipid accumulation. Aminguanidine significantly reduces the cholesterol, Triglycerides, Low density lipoproteins in Streptozotocin induced diabetic mice and reduces accumulated Triglycerides and Phospholipids in cell lysates of H9C2 exposed to high glucose and Aminoguanidine. Exact mechanisms responsible for the high glucose induced lipid accumulation and by which lipotoxicity alter cardiac structure and function are incompletely understood. This study mainly focuses on cardio protective antilipidemic activity of Aminguanidine against streptozotocin induced diabetic heart and high glucose induced lipid synthesis in H9C2 cardiac myoblasts.