Key result
GBE50 combined with aspirin displayed synergistic antiplatelet effects in arachidonic acid-induced platelet aggregation and additive effects in PAF, ADP, and collagen-induced aggregation in vitro.
Why the study?
Does the combination of Ginkgo biloba extract 50 and aspirin reduce platelet aggregation in vitro?
Does the combination of Ginkgo biloba extract 50 and aspirin reduce platelet aggregation in vitro?
GBE50 combined with aspirin exerts synergistic and additive antiplatelet effects in vitro, highlighting its potential as a supplementary therapy for thrombosis-related diseases.
In vitro synergy data leaves open any clinical antiplatelet benefit of GBE50 plus aspirin; human trials needed.
PURPOSE: extract (GBE50) in combination with aspirin using in vitro models. METHODS: Arachidonic acid (AA), platelet activating factor (PAF), adenosine 5'-diphosphate (ADP) and collagen were used as inducers. The antiplatelet effects of GBE50, aspirin and 1:1 combination of GBE50 and aspirin were detected by microplate method using rabbit platelets. Synergy finder 2.0 was used to analyze the synergistic antiplatelet effect. The compounds in GBE50 were identified by UPLC-Q/TOF-MS analysis and the candidate compounds were screened by TCMSP database. The targets of candidate compounds and aspirin were obtained in TCMSP, CCGs, Swiss target prediction database and drugbank. Targets involving platelet aggregation were obtained from GenCLiP database. Compound-target network was constructed and GO and KEGG enrichment analyses were performed to identify the critical biological processes and signaling pathways. The levels of thromboxane B2 (TXB2), cyclic adenosine monophosphate (cAMP) and PAF receptor (PAFR) were detected by ELISA to determine the effects of GBE50, aspirin and their combination on these pathways. RESULTS: GBE50 combined with aspirin inhibited platelet aggregation more effectively. The combination displayed synergistic antiplatelet effects in AA-induced platelet aggregation, and additive antiplatelet effects occurred in PAF, ADP and collagen induced platelet aggregation. Seven compounds were identified as candidate compounds in GBE50. Enrichment analyses revealed that GBE50 could interfere with platelet aggregation via cAMP pathway, AA metabolism and calcium signaling pathway, and aspirin could regulate platelet aggregation through AA metabolism and platelet activation. ELISA experiments showed that GBE50 combined with aspirin could increase cAMP levels in resting platelets, and decreased the levels of TXB2 and PAFR. CONCLUSION: Our study indicated that GBE50 combined with aspirin could enhance the antiplatelet effects. They exerted both synergistic and additive effects in restraining platelet aggregation. The study highlighted the potential application of GBE50 as a supplementary therapy to treat thrombosis-related diseases.
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Ke et al. (2021) studied Platelet aggregation. GBE50 combined with aspirin vs. GBE50 alone and aspirin alone was evaluated on Platelet aggregation. GBE50 combined with aspirin displayed synergistic antiplatelet effects in arachidonic acid-induced platelet aggregation and additive effects in PAF, ADP, and collagen-induced aggregation in vitro.
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