Background: Immune thrombocytopenia (ITP) is a heterogeneous autoimmune disease characterized by platelet destruction. In previous studies, Jianpi Yiqi Shexue (JPYQSX) was shown to increase the peripheral platelet (PLT) counts in patients with ITP. In addition, JPYQSX also dramatically alleviated weakness and fatigue. This study aimed to investigate the effect of JPYQSX on ITP related fatigue and to illuminate the underlying mechanisms of its therapeutic effects. Methods: Prednisone and different doses of JPYQSX were orally administered to mice with ITP. Posttreatment, all mice were subjected to a forced swimming test. In addition, blood samples were analyzed using an automated hematology analyzer. Spleen, liver, lungs, heart, kidneys, and colon tissues were collected to determine the expressions of reactive oxygen species (ROS), adenosine triphosphate (ATP), mitochondrial DNA (mtDNA), succinate dehydrogenase complex flavoprotein subunit A (SDHA), caseinolytic mitochondrial matrix peptidase proteolytic subunit (ClpP), and Lon peptidase 1 (Lonp1). Results: Compared with the vehicle group, JPYQSX prolonged the forced swimming time, increased the PLT counts, and reduced the liver and spleen indices {calculated as follows: organ index (%) = [organ weight (mg)/body weight (g)] ×100%}. In addition, the levels of ROS were upregulated, while the ATP and mtDNA contents were downregulated in ITP model mice. Administration of JPYQSX restored the expression of these mitochondrial molecules to normal levels. Furthermore, JPYQSX also decreased the expressions of SDHA, ClpP, and Lonp1, which are closely related to mitochondrial activity. Conclusions: These findings suggest that JPYQSX prevents antiplatelet sera-mediated platelet destruction in ITP mice and ameliorates fatigue possibly through its effect on mitochondrial function. This study revealed JPYQSX as a potential alternative approach for ITP therapy.

Background: To explore the effect mechanism of "treat the spleen" therapy on immune thrombocytopenia (ITP) based on the characteristics of vasoactive factors.Methods: The ITP mice model was established by passive immunomodeling. 120 successfully modeled BALB/c mice were randomly divided into 6 groups: normal group, model group, prednisone group, Guipi Decoction group, Jianpi Yiqi group, and Jianpi Shexue group. These mice were treated with medicine for 16 days. After treatment, the platelet (PLT) counts and the degree of bleeding were evaluated, and the serum ET-1, NO, NOS3, TXA2, PGI2, vWF, VCAM-1, and TM contents of the model mice were detected by enzyme-linked immunosorbent assay (ELISA). Results:The PLT counts in peripheral blood of mice in each experimental group significantly decreased compared with that in the normal group (P<0.01). On the 8th day after commencing administration, compared with the model group, PLT counts of mice in each experimental group significantly increased (P<0.01). Before administration, all groups had different bleeding tendencies except for the normal group.On the 6th and 8th day of drug intervention, compared with the model group, the bleeding grade of treated groups was significantly decreased (P<0.01). The values of ET-1, vWF, and VCAM-1 in each experimental group significantly decreased compared with that in the normal group, while the TXA2 values were up-regulated compared with that in the normal and model groups (P<0.01). The values of NO and TM in each experimental group significantly decreased compared with that in the normal group (P<0.05).In addition to the Guipi Decoction group, the NOS3 values in each group were significantly decreased compared with that in the normal group (P<0.05). The PGI2 values of the "treat the spleen" groups were significantly decreased compared to the normal group (P<0.01). Conclusions:In addition to increasing the PLT counts in peripheral blood of ITP model mice to achieve a hemostatic effect, the "treat the spleen" recipes up-regulated the levels of TXA2 and VCAM-1, while down-regulating the levels of PGI2 and TM. Therefore, balancing the procoagulant and anticoagulant factors might be one of the effective mechanisms of hemostasis.