Antiplatelet Effect of Active Components Derived from Chinese Herbal Medicine

Zhang, Ying; Ma, Xiao‐Jun; Shi, Dazhuo

doi:10.1007/s11655-015-2297-9

Cited by 4 publications

(2 citation statements)

References 40 publications

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“…There is growing interest in natural bioactive components that suppress platelet function isolated from Chinese herbs and natural plants [ 13 ]. Interestingly, some may exert an inhibitory effect on platelet activation by modulating membrane receptor-related signaling pathways.…”

Section: Introductionmentioning

confidence: 99%

Antiplatelet Activity of Tetramethylpyrazine via Regulation of the P2Y12 Receptor Downstream Signaling Pathway

Guan

Gao

Tan

et al. 2022

Evidence-Based Complementary and Alternative Medicine

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Background. Tetramethylpyrazine (TMP) is an alkaloid in Chinese herbal medicine, which possesses antiplatelet activity. TMP inhibits platelet activation in many ways. The platelet P2Y12 receptor for adenosine 5′ diphosphate (ADP) plays a central role in platelet function, hemostasis, and thrombosis. Here, we investigated the inhibitory effect of TMP on P2Y12 receptor-related platelet function. Methods. The inhibitory potential of TMP was assessed using agonist-induced platelet aggregation, flow cytometric analysis of CD62p expression, PAC-1 activation, and fibrin clot retraction. After the P2Y12 receptor-related signaling pathway was inhibited using the blocker, platelet activation was studied by platelet aggregation, CD62p expression, and PAC-1 activation. The secretion of cyclic adenosine monophosphate (cAMP) was measured using enzyme-linked immunosorbent assay (ELISA), and the expression of signaling pathway protein, phosphorylation of vasodilator-stimulated phosphoprotein, and phosphorylation of Akt were investigated using western blotting. The release of platelet inflammatory mediators was measured using ELISA. Results. TMP had an antiplatelet effect by inhibiting ADP-induced aggregation, P-selectin secretion, and glycoprotein (GP) IIb/IIIa expression and reducing the release of atherosclerotic-related inflammatory mediators (sCD40L and IL-1β). TMP decreased the area of clot retraction, reflecting inhibition of GPIIb/IIIa activation. TMP inhibited adenosine diphosphate-induced platelet activation via increased cAMP production, VASPser157 phosphorylation, and Akt dephosphorylation. Conclusion. TMP selectively inhibits ADP-induced platelet activation via P2Y12 receptor-related signaling pathways.

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Section: Introductionmentioning

confidence: 99%

Antiplatelet Activity of Tetramethylpyrazine via Regulation of the P2Y12 Receptor Downstream Signaling Pathway

Guan

Gao

Tan

et al. 2022

Evidence-Based Complementary and Alternative Medicine

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“…Recently, plenty of antiplatelet inhibitors have been isolated from natural sources (Santhakumar, Stanley, & Singh, 2015; Su, Su, He, Ming, & Kong, 2015; Zhang, Tan, et al, 2018; Zhang, Ma, & Shi, 2018). Collagen peptide is the product of enzymatic degradation of collagen, which usually result in characteristics such as easy absorption, low immunogenicity, safety, and less toxic side effects.…”

Section: Introductionmentioning

confidence: 99%

A novel di‐peptide Met‐Glu from collagen hydrolysates inhibits platelet aggregation and thrombus formation via regulation of Gq‐mediated signaling

et al. 2020

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Increasing evidence has shown that collagen peptides had various biological activities. In this study, a novel antiplatelet peptide Met‐Glu (ME) was separated and identified from silver carp skin by YMC ODS‐A C18 separation and ESI‐MS/MS analysis. Peptide ME inhibited platelet aggregation and secretion of platelet granules induced by ADP, thrombin and collagen, and significantly attenuated ferric chloride‐induced thrombus formation in rats. It did not prolong the bleeding time in mice even at the dose of 300 μmol/kg body weight that showed potent anti‐thrombosis effects. Additionally, peptide ME targeted at Gq‐protein to downregulate the phosphorylation of PLCβ, an important upstream effector of PI3K/Akt and Erk/MAPK signaling to inhibit intracellular calcium ion mobilization. These results suggest that peptide ME inhibited thrombosis in vivo and inhibited Gq‐mediated signaling in platelets, indicating the possibility that ME could potentially be developed as a novel therapeutic agent in the prevention and treatment of thrombotic diseases. Practical applications Cardiovascular diseases (CVDs) are the leading cause of mortality and morbidity worldwide. The proximal cause of CVDs is intravascular thrombosis formation, which mostly results from platelet activation, aggregation, and granules secretion. Traditional drugs in the prevention of thrombotic disease, such as aspirin and clopidogrel, are still limited for their side effects, especially bleeding complications. Collagen is a natural source for bioactive peptides and our previous study has shown that collagen peptides could inhibit platelet aggregation in vitro. Understanding the mechanism of collagen peptides on regulation of platelet activation and their in vivo anti‐thrombosis activities were important for the development of novel‐specific medical food in the prevention of thrombotic diseases.

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