Abstract
Morin hydrate, a bioactive flavonoid, has been proven to prevent inflammation and apoptosis of cells. Flavonoids can reduce the risk of cardiovascular diseases, in which platelet activation plays a major role. This study investigated the effect of morin hydrate on platelet activation in vitro and in vivo. Morin hydrate markedly inhibited platelet aggregation stimulated by collagen in human platelets but not that stimulated by other agonists. In collagen-activated platelets, morin hydrate inhibited adenosine triphosphate (ATP) release; intracellular Ca2+ mobilization; P-selectin expression; and phosphorylation of phospholipase Cγ2 (PLCγ2), protein kinase C (PKC), and Akt. In mitogen-activated protein kinase (MAPK) activation, morin hydrate evidently diminished ERK2 or JNK1 activation, except for p38 MAPK. Additionally, morin hydrate markedly reduced the OH· signals in platelet suspensions but not in the cell-free system (Fenton reaction solution). Moreover, morin hydrate substantially increased the occlusion time of thrombotic platelet plug formation but had no effect on bleeding time in mice. In conclusion, morin hydrate crucially inhibits platelet activation through inhibition of the PLCγ2–PKC cascade and subsequent suppression of Akt and MAPK activation, thereby ultimately inhibiting platelet aggregation. Therefore, this paper suggests that morin hydrate constitutes a novel and potential natural therapeutic product for preventing or treating thromboembolic disorders.
Highlights
Flavonoids are naturally occurring compounds that contain a number of phenolic hydroxyl groups attached to ring structures designated as A, B, and C (Figure 1A)
Morin hydrate (20, 50, and 80 μM; Figure 1B,C) strongly inhibited platelet aggregation stimulated by 1 μg/mL of collagen but not by 0.01 U/mL of thrombin, 1 μM of U46619, a prostaglandin endoperoxide, or arachidonic acid (AA) (60 μM)
Morin hydrate effectively inhibited platelet aggregation stimulated by collagen but not that stimulated by thrombin, AA, or U46619, indicating that this compound inhibits platelet aggregation through a markedly Phospholipase C (PLC)-dependent mechanism
Summary
Flavonoids are naturally occurring compounds that contain a number of phenolic hydroxyl groups attached to ring structures designated as A, B, and C (Figure 1A). The structure of flavonoids usually characterized by two aromatic rings (A and B) joined by a three-carbon linked C-pyrone ring is usually characterized by two aromatic rings (A and B) joined by a three-carbon linked C-pyrone (C) to form a C6–C3–C6 skeletal unit (Figure 1A). The bioactivity of flavonoids has attracted academic ring (C) to form a C6–C3–C6 skeletal unit (Figure 1A). The bioactivity of flavonoids has attracted interest because of its potential health benefits for humans. Diets rich in fruits and vegetables exert academic interest because of its potential health benefits for humans. Diets rich in fruits and protective effects cardiovascular (CVDs)diseases and certain forms of cancer [1].ofFlavonoids vegetables exertagainst protective effects againstdiseases cardiovascular (CVDs) and certain forms cancer have been used as valuable therapeutic agents in modern and traditional medicine
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