Objective To observe the activation function of peripheral blood platelets in a mouse model of immune thrombocytopenia ( ITP) with qi failing to control blood syndrome. Methods BALB/ c mice were randomly divided into control and model groups. The model group was subjected to sleep deprivation for one week, followed by two weeks of sleep deprivation combined with intraperitoneal injection of anti-platelet serum to replicate an ITP mouse model with qi failing to control blood syndrome. At the end of the experimental period, the morphology of platelets isolated from the mice was observed by a scanning electron microscope. Moreover, ELISA was used to detect the release of platelet alpha particles (β-TG, PF-4) and dense granules (ATP, ADP). Flow cytometry was used to detect CD62P expression, platelet- neutrophil aggregation (PNA), mitochondrial membrane potential (MMP), and the mean fluorescence intensity of reactive oxygen species (ROS-MFI). Results The platelets from the control group were mostly round or disk-like with a small degree of pseudopodia formation, while platelets from the model group were mostly irregular in shapes, with a large degree of pseudopodia formation, and some of them adhered and aggregated into groups. Compared with the control group, β-TG, PF-4, ATP, MMP, and ROS-MFI in the model group were significantly increased (P <0. 01), while CD62P, ADP, and PNA were increased significantly, but to a lesser extent (P <0. 05). Conclusions Platelets from the peripheral blood of a mouse model of ITP with qi failing to control blood syndrome were highly activated and exhibited increased rates of apoptosis compared with control mice.