» Articles » PMID: 39563013

Selective Inhibition of P2Y and P2Y Receptor Signal Pathways in Platelet Aggregation in Transgenic Cell Lines and Rats by Potassium 2-(1-Hydroxypentyl)-Benzoate, Puerarin and Salvianolic Acid B

Overview
Specialties Neurology
Pharmacology
Date 2024 Nov 20
PMID 39563013
Authors
Affiliations
Soon will be listed here.
Abstract

Aim: Potassium 2-(1-hydroxypentyl)-benzoate (dl-PHPB), puerarin and salvianolic acid B are three natural products or derivatives that can inhibit platelet aggregation. However, the mechanisms of dl-PHPB, puerarin and salvianolic acid B to inhibit platelet aggregation are still not clear.

Method: Here, 2-methylthioadenosine diphosphate (2-MeSADP) was used as an inducer to confirm the effects of three drugs on platelet aggregation and illustrate the corresponding mechanisms.

Result: The results indicated that dl-PHPB, puerarin and salvianolic acid B significantly inhibited platelet aggregation both in vivo and in vitro. In addition, the content of IP, cAMP and intracellular [Ca] were measured in HEK293 cell lines overexpressing P2Y and P2Y. Dl-PHPB and puerarin could obviously reduce 2-MeSADP-induced IP increase, but salvianolic acid B showed no effects. Unlike dl-PHPB and puerarin, which had no effects on 2-MeSADP-induced cAMP decrease, salvianolic acid B significantly reversed the reduction of cAMP. Both dl-PHPB and puerarin could decrease the enhanced intracellular [Ca] induced by 2-MeSADP; however, salvianolic acid B showed no effect on intracellular [Ca] elevation.

Conclusion: These results suggested that dl-PHPB and puerarin inhibited platelet aggregation via targeting at P2Y receptor and P2Y-Gq-IP-Ca signal pathway. Differently, salvianolic acid B inhibited platelet aggregation via targeting at P2Y receptor and via Gi-AC-cAMP signal pathway.

References
1.
Qi R, Liao F, Inoue K, Yatomi Y, Sato K, Ozaki Y . Inhibition by diallyl trisulfide, a garlic component, of intracellular Ca(2+) mobilization without affecting inositol-1,4, 5-trisphosphate (IP(3)) formation in activated platelets. Biochem Pharmacol. 2000; 60(10):1475-83. DOI: 10.1016/s0006-2952(00)00467-6. View

2.
. A randomised, blinded, trial of clopidogrel versus aspirin in patients at risk of ischaemic events (CAPRIE). CAPRIE Steering Committee. Lancet. 1996; 348(9038):1329-39. DOI: 10.1016/s0140-6736(96)09457-3. View

3.
Li S, Feng X, Xu H, Chen K . Comparison on Anticoagulation and Antiplatelet Aggregation Effects of Puerarin with Heparin Sodium and Tirofiban Hydrochloride: An In Vitro Study. Chin J Integr Med. 2017; 24(2):103-108. DOI: 10.1007/s11655-017-2419-7. View

4.
. Collaborative overview of randomised trials of antiplatelet therapy--I: Prevention of death, myocardial infarction, and stroke by prolonged antiplatelet therapy in various categories of patients. Antiplatelet Trialists' Collaboration. BMJ. 1994; 308(6921):81-106. PMC: 2539220. View

5.
Guan B, Gao J, Tan Y, Ma X, Shi D . Antiplatelet Activity of Tetramethylpyrazine via Regulation of the P2Y12 Receptor Downstream Signaling Pathway. Evid Based Complement Alternat Med. 2022; 2022:7941039. PMC: 8976642. DOI: 10.1155/2022/7941039. View