Effect of Bile on Aggregation and Morphology of Rabbit Platelets

Takano, Shizuko; Suzuki, Takehiko

doi:10.1620/tjem.131.71

Cited by 3 publications

(1 citation statement)

References 7 publications

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“…Taurine and related compounds have been repeatedly pointed as modulating factors of platelet function [113,119], but the interest regarding their influence on blood coagulation dates from the early 1950s and 1960s [120,121]. Research on taurine effects over hemostasis started with the observation that bile acids (such as taurocholic, taurodeoxycholic, or taurochenodeoxycholic acid) and their salts elicit a considerable inhibition on platelet aggregation induced by various agonists (ADP, collagen, and others) [122][123][124][125]. It has been assumed that a probable impaired platelet aggregation in the upper segment of the gastrointestinal tract induced by biliary reflux might partly explain the poor hemostatic response in these otherwise normal human subjects [122].…”

Section: Taurine Influence On Platelet Hemostatic Activitymentioning

confidence: 99%

Taurine and Its Derivatives: Analysis of the Inhibitory Effect on Platelet Function and Their Antithrombotic Potential

Roşca

Vlădăreanu

Mirică

et al. 2022

JCM

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Taurine is a semi-essential, the most abundant free amino acid in the human body, with a six times higher concentration in platelets than any other amino acid. It is highly beneficial for the organism, has many therapeutic actions, and is currently approved for heart failure treatment in Japan. Taurine has been repeatedly reported to elicit an inhibitory action on platelet activation and aggregation, sustained by in vivo, ex vivo, and in vitro animal and human studies. Taurine showed effectiveness in several pathologies involving thrombotic diathesis, such as diabetes, traumatic brain injury, acute ischemic stroke, and others. As human prospective studies on thrombosis outcome are very difficult to carry out, there is an obvious need to validate existing findings, and bring new compelling data about the mechanisms underlying taurine and derivatives antiplatelet action and their antithrombotic potential. Chloramine derivatives of taurine proved a higher stability and pronounced selectivity for platelet receptors, raising the assumption that they could represent future potential antithrombotic agents. Considering that taurine and its analogues display permissible side effects, along with the need of finding new, alternative antithrombotic drugs with minimal side effects and long-term action, the potential clinical relevance of this fascinating nutrient and its derivatives requires further consideration.

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Section: Taurine Influence On Platelet Hemostatic Activitymentioning

confidence: 99%

Taurine and Its Derivatives: Analysis of the Inhibitory Effect on Platelet Function and Their Antithrombotic Potential

Roşca

Vlădăreanu

Mirică

et al. 2022

JCM

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Mechanism of Bile Acid in Regulating Platelet Function and Thrombotic Diseases

Zhou,

Zhang

et al. 2024

Advanced Science

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Platelets play a key role in physiological hemostasis and pathological thrombosis. Based on the limitations of current antiplatelet drugs, it's important to elucidate the mechanisms of regulating platelet activation. In addition to dissolving lipid nutrients, bile acids (BAs) can regulate platelet function. However, the specific mechanisms underlying BAs‐mediated effects on platelet activation and thrombotic diseases remain unknown. Therefore, the effects of BAs on platelets and intracellular regulatory mechanisms are explored. It is showed that the inhibitory effect of secondary BAs is more significant than that of primary BAs; lithocholic acid (LCA) shows the highest inhibitory effect. In the process of platelet activation, BAs suppress platelet activation via the spleen tyrosine kinase (SYK), protein kinase B (Akt), and extracellular signal‐regulated kinase1/2 (Erk1/2) pathways. Nck adaptor proteins (NCK1) deficiency significantly suppress the activity of platelets and arterial thrombosis. Phosphorylated proteomics reveal that LCA inhibited phosphorylation of syntaxin‐11 at S80/81 in platelets. Additional LCA supplementation attenuated atherosclerotic plaque development and reduced the inflammation in mice. In conclusion, BAs play key roles in platelet activation via Syk, Akt, ERK1/2, and syntaxin‐11 pathways, which are associated with NCK1. The anti‐platelet effects of BAs provide a theoretical basis for the prevention and therapy of thrombotic diseases.

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