Down-regulation of SCAP inhibits cardiomyocyte injury induced by high glucose

Diabetic cardiomyopathy (DCM) is a type of myocardial injury induced by diabetes. Under the stimulation of continuous hyperglycemia, cardiomyocytes will produce a series of stress responses include apoptosis and inflammation. Sterol regulatory element binding protein cleavage-activating protein (SCAP) is a cholesterol-regulating protein, which is related to diabetes and is abnormally expressed in a variety of complications of diabetes. The purpose of this study was to explore the role of SCAP on cardiomyocyte injury. H9C2 cells were exposed to 35 mmol glucose for 48 h to induce myocardial injury. The results of western blot and immunofluorescence staining showed that the expression of SCAP was increased in high glucose stimulated cells and cardiomyocyte apoptosis increased obviously after high glucose intervention. Then we transfected SCAP siRNA to inhibit SCAP. Our results showed that apoptosis of H9C2 cells induced by high glucose alleviated significantly after SCAP was silenced. And down-regulation of SCAP could also restrained reactive oxygen species (ROS) induced by high glucose. Meanwhile, the protein levels of NLRP3, Caspase-1, IL-1β, and p-NF-κB protein was decreased. This reminds us that down-regulation of SCAP can inhibit the apoptosis, ROS and inflammation of cardiomyocytes induced by high glucose. The above evidence speculates that SCAP might play a potential role in the cardiomyocytes injury under high glucose surroundings.