Authors: Yi Chang, Yi-Ju Chen, Joen-Rong Sheu, Wei-Chieh Huang, Chih-Wei Hsia.
Metformin is extensively prescribed as a first-line medication for the management of type 2 diabetes (T2D), a condition frequently coexisting with kidney disease, cardiovascular diseases (CVDs), and retinopathy. The widespread use of metformin is attributed to its well-established safety profile. Notably, platelets play a crucial role in arterial thrombosis, a significant factor contributing to the development of CVDs and cerebrovascular diseases. Our previous study has demonstrated that metformin may reduce collagen-induced platelet activation in human subjects, indicating a positive impact on platelet function. However, its mechanisms in platelet activation stimulated by other agonists remain not fully understood, especially regarding the effect of metformin on thrombininduced platelet activation. In this study, metformin inhibited platelet aggregation stimulated by thrombin in a concentration-dependent manner. Metformin suppressed P-selectin expression, [Ca2+]i mobilization, ATP-release, and as well as protein kinase C (PKC), Akt and p38 mitogen-activated protein kinase (MAPK). In conclusion, metformin can potentially function as a nutritional agent for long-term use at a low dose to prevent cardiovascular diseases (CVDs) or other chronic diseases.
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