Hinokitiol inhibits platelet activation ex vivo and thrombus formation in vivo.

Hinokitiol is a tropolone-related bioactive compound that has been used in hair tonics, cosmetics, and food as an antimicrobial agent. Recently, hinokitiol has attracted considerable interest because of its anticancer activities. Platelet activation plays a crucial role in atherothrombotic processes.

Suppression of NF-κB signaling by andrographolide with a novel mechanism in human platelets: regulatory roles of the p38 MAPK-hydroxyl radical-ERK2 cascade.

Andrographolide, a novel nuclear factor-κB (NF-κB) inhibitor, is isolated from leaves of Andrographis paniculata. Platelet activation is relevant to a variety of coronary heart diseases. Our recent studies revealed that andrographolide possesses potent antiplatelet activity by activating the endothelial nitric oxide synthase (eNOS)-NO-cyclic GMP pathway.

A novel role for tamoxifen in the inhibition of human platelets.

Tamoxifen, a selective estrogen receptor (ER) modulator (SERM), is widely used therapeutically for the treatment and prevention of breast cancer, but its use is associated with an increased risk of thrombosis. The mechanism of this adverse effect is still unclear. Arterial thromboses mostly consist of platelets that are adherent to ruptured endothelial surfaces.

Arsenic trioxide-mediated antiplatelet activity: pivotal role of the phospholipase C gamma 2-protein kinase C-p38 MAPK cascade.

Arsenic trioxide produces high rates of complete clinical remission in patients with relapsed/refractory acute promyelocytic leukemia. Platelet activation is relevant in a variety of acute thrombotic events and coronary heart diseases. Few studies have examined the effects of arsenic trioxide on platelets, and the mechanisms underlying the signaling pathways remain obscure.

Potent antiplatelet activity of sesamol in an in vitro and in vivo model: pivotal roles of cyclic AMP and p38 mitogen-activated protein kinase.

Sesamol is a potent phenolic antioxidant which possesses antimutagenic, antihepatotoxic and antiaging properties. Platelet activation is relevant to a variety of acute thrombotic events and coronary heart diseases. There have been few studies on the effect of sesamol on platelets.

Mechanisms of resveratrol-induced platelet apoptosis.

Aims: Apoptotic events have recently been found to occur in platelets, which are anuclear. Resveratrol is present in red wine and has various biological activities, including inhibition of platelet aggregation. Although considerable evidence is available as to the induction of tumour cell apoptosis by resveratrol, resveratrol's effects on platelet apoptosis have not yet been investigated.

Amyloid beta peptide-activated signal pathways in human platelets.

Amyloid beta peptide (amyloid-beta), which accumulates in the cerebral microvessels in an age-dependent manner, plays a key role in the pathogenesis of cerebral amyloid angiopathy. Platelets are an important cellular element in vasculopathy of various causes. Amyloid-beta may activate or potentiate platelet aggregation.

Inhibitory mechanisms of resveratrol in platelet activation: pivotal roles of p38 MAPK and NO/cyclic GMP.

Resveratrol has been reported to have antiplatelet activity; however, the detailed mechanisms have not yet been resolved. This study aimed to systematically examine the detailed mechanisms of resveratrol in the prevention of platelet activation in vitro and in vivo. Resveratrol (0.

Characterization of a novel and potent collagen antagonist, caffeic acid phenethyl ester, in human platelets: in vitro and in vivo studies.

Objective: Caffeic acid phenethyl ester (CAPE), which is derived from the propolis of honeybee hives, has been demonstrated to possess multiple pharmacological activities. In the present study, CAPE (6-25 microM) specifically inhibited collagen-induced platelet aggregation and the ATP release reaction in platelet suspensions.

Methods: Platelet aggregation, flow cytometric analysis, immunoblotting, and electron spin resonance (ESR) were used to assess the anti-platelet activity of CAPE.

Protective mechanisms of inosine in platelet activation and cerebral ischemic damage.

Objective: Inosine is a naturally occurring nucleoside degraded from adenosine. Recent studies have demonstrated that inosine has potent immunomodulatory and neuroprotective effects. In the present study, we further investigated the inhibitory effects of inosine on platelet activation in vitro and in vivo, as well as in attenuating middle cerebral artery occlusion (MCAO)-induced focal cerebral ischemia in rats.

A potent antioxidant, lycopene, affords neuroprotection against microglia activation and focal cerebral ischemia in rats.

We investigated the effects of a potent antioxidant, lycopene, on the free radical-scavenging activity as evaluated by the DPPH test and lipid peroxidation in rat brain homogenates as well as nitric oxide (NO) formation in cultured microglia stimulated by lipopolysaccharide. In addition, we also investigated the therapeutic effect of lycopene in attenuating ischemia/reperfusion brain injury induced by middle cerebral artery (MCA) occlusion in rats. Lycopene (1, 2 and 5 microM) exerted increased DPPH decolorization in the DPPH test, and increased inhibition of iron-catalyzed lipid peroxidation (TBARS formation) in rat brain homogenates in concentration-dependent manners.

Inhibitory mechanisms of metallothionein on platelet aggregation in in vitro and platelet plug formation in in vivo experiments.

Metallothionein (MT) is a low-molecular-weight, cysteine-rich protein that contains heavy metals such as cadmium and zinc. The biological function of MT in platelets is not yet understood. Therefore, the aim of this study was to systematically examine the inhibitory mechanisms of metallothionein in platelet aggregation.

Mechanisms involved in the antiplatelet activity of midazolam in human platelets.

Background: Midazolam is widely used as a sedative and anesthetic induction agent. The aim of this study was to systematically examine the inhibitory mechanisms of midazolam in platelet aggregation.

Methods: The inhibitory mechanisms of midazolam in platelet aggregation were explored by means of analysis of the platelet glycoprotein IIb-IIIa complex, phosphoinositide breakdown, intracellular Ca+2 mobilization, measurement of membrane fluidity, thromboxane B2 formation, and protein kinase C activity.