Anti-thrombotic activity of fermented rice bran extract with several oriental plants in vitro and in vivo.
10.14405/kjvr.2015.55.4.233
- Author:
Bo Ra JEON
1
;
Hyun Dong JI
;
Su Jung KIM
;
Chun Hee LEE
;
Tae Wan KIM
;
Man Hee RHEE
Author Information
1. Laboratory of Veterinary Physiology and Cell Signaling, College of Veterinary Medicine, Kyungpook National University, Daegu 41566, Korea. rheemh@knu.ac.kr
- Publication Type:In Vitro ; Original Article
- Keywords:
collagen;
mitogen-activated protein kinase;
platelet aggregation;
rice bran;
thrombosis
- MeSH:
Adenosine Triphosphate;
Angelica;
Animals;
Blood Platelets;
Calcium;
Camellia;
Cardiovascular Diseases;
Cnidium;
Collagen;
Fibrinogen;
Functional Food;
JNK Mitogen-Activated Protein Kinases;
Phosphorylation;
Phosphotransferases;
Physiology;
Platelet Aggregation;
Platelet Glycoprotein GPIIb-IIIa Complex;
Protein Kinases;
Rats;
Thrombosis
- From:Korean Journal of Veterinary Research
2015;55(4):233-240
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
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 alphaIIbbeta3 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 concentration-dependent 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.
