Research Projects

Diabetes mellitus (DM) is a significant risk factor for ischemic stroke, with excessive glucose uptake by platelets during DM stroke increasing the risk of bleeding and thrombocytopenia. Antiplatelet use minimizes diabetes-associated coagulative risks, but there is a need to reduce these risks. The GLUT3 transporter regulates glucose entry and exit into platelets and neurons, and hyperglycemia promotes glucose entry, leading to diabetic stroke. Simultaneously ameliorating glucose and platelet aggregation could be a promising therapeutic strategy to combat diabetes-associated platelet dysfunction and brain-related neurological issues. The study aims to prevent platelet dysfunction and protect the brain from DM and its comorbid ischemic stroke. Hypothesis: Hyperglycemia promotes glucose uptake by platelets and brain via GLUT1&3. Glucose is utilized by mitochondria, releasing more ATP and ROS. ROS cause endothelium damage in blood vessels, releasing Endothelin-1 and decreasing NO and PGI2. Glucose entry into the brain causes brain mitochondrial damage, inflammation, and apoptosis of neurons. The administration of I3C and DIM can mitigate hyperglycemia, platelet aggregation, inflammation, oxidative stress, and mitochondrial dysfunction in DM and its associated ischemic stroke. Experiments will involve induced diabetes mellites in rat STZ/NA injections, and protective roles will be evaluated by measuring platelet glucose metabolism, platelet aggregation, and platelet mitochondrial function in diabetic and diabetic stroke animals. This study aims to create a roadmap for researchers to focus on platelet glucose metabolism to stop coagulate risks in diabetic patients and develop new therapeutic opportunities against diabetic stroke.