Although the effects of the rice bran have recently been investigated, there is no information regarding platelet physiology available. However, it is well known that fermented natural plants have a beneficial effect on cardiovascular diseases. Therefore, this study was conducted to investigate whether fermented rice bran extract (FRBE) with several plants (Artemisia princeps, Angelica Gigantis Radix, Cnidium officinale, and Camellia sinensis) affected agonist - induced platelet aggregation, and if so, what the underlying mechanism of its activity was. We performed several experiments, including in vitro platelet aggregation, intracellular calcium concentration and adenosine triphosphate release. In addition, the activation of integrin alpha IIb beta3 was determined using fibrinogen binding. Thrombus formation was also evaluated in vivo using an arterio-venous shunt model. The FRBE inhibited collagen-induced platelet aggregation in a concentrationdependent manner. FRBE significantly and dose dependently attenuated thrombus formation using rat arterio-venous shunt. FRBE suppressed the intracellular calcium mobilization in collagen-stimulated platelets. We also found that FRBE inhibited extracellular stimuli-responsive kinase 1/2, p38-mitogen - activated protein kinases and c-Jun N-terminal kinase phosphorylation. These results suggested that FRBE inhibited collagen-induced platelet aggregation, which was mediated by modulation of downstream signaling molecules. In conclusion, FRBE could be developed as a functional food against aberrant platelet activation-related cardiovascular diseases.

The objective of this study was to investigate the changes in synovial fluid concentration of collagen type II cleavage site (C2C) and pro collagen II C-propeptide (CPII), markers of joint cartilage degeneration and synthesis, respectively, in horses with intraarticular fracture or osteochondrosis dissecans (OCD), and to examine the relationship between arthroscopic findings and these biomarker levels. Synovial fluid was collected from 36 joints in 18 horses (6 fractures and 12 OCDs). Samples from contralateral normal joints, when available, served as controls (n=12). Concentrations of C2C and CPII were measured using enzyme-linked immunosorbant assays. Moreover, the severity of the cartilage degradation was graded arthroscopically in 16 horses, and the correlation between the C2C and CPII levels and the arthroscopic scores were investigated. Compared to the control, the concentration of C2C was increased in OCD joints but not in fracture joints, whereas the concentration of CPII was increased in fracture joints but not in OCD joints. Within each disease group there was no correlation between biomarker levels and arthroscopic findings. Therefore, although C2C and CPII have diagnostic potential further knowledge is required to provide accurate analysis.