Key result
Momordica charantia exosomes inhibit platelet activation and reduce thrombus agglutination in preclinical testing.
Why the study?
The effects of Momordica charantia exosomes on platelet activation, adhesion, and aggregation were not previously studied, despite platelets' role in stroke and tumor metastasis.
Do Momordica charantia exosomes inhibit platelet activation, adhesion, and aggregation in preclinical models?
Do Momordica charantia exosomes inhibit platelet activation, adhesion, and aggregation in preclinical models?
Momordica charantia exosomes inhibit platelet activation, adhesion, and aggregation, suggesting potential therapeutic utility in conditions like stroke and tumor metastasis.
Answers are grounded in this paper and cite their sources.
Hypothesis-generating for Momordica charantia exosomes as antiplatelet agents; leaves open human translation and safety.
The platelets play a crucial role in the progression of multiple medical conditions, such as stroke and tumor metastasis, where antiplatelet therapy may be a boon for treating these diseases. In this study, we have attempted to study the effects of extracted Momordica charantia exosomes (MCEs) on platelet activation, adhesion, and aggregation. Adult platelets isolated from healthy individuals were dose-dependently treated with MCEs (0.1, 40, and 200 μg/ml). We performed flow cytometry to detect the expression of platelet activation protein marker-activated GP IIb/IIIa (PAC-1) and P-selectin (CD62P). Platelet adhesion was analyzed through fluorescence labeling assays. The effect of MCEs on platelet-mediated cell migration of HCT116 cells was observed by transwell. Furthermore, the MCAO model of Sprague-Dawley rats was used to observe the effect of MCEs (200, 400, and 800 μg/kg) on platelet aggregation and maximum thrombotic agglutination in vivo . The results showed that 200 μg/ml MCEs exerted the most pronounced effect on platelet activation, adhesion, and aggregation. Experiments on animals showed that MCEs significantly inhibited platelet aggregation and attenuated the maximum thrombus agglutination. We concluded that MCEs inhibited platelet activation, adhesion, aggregation, and platelet-mediated migration of HCT116 cells, indicating the potential role MCEs may play in the treatment of stroke and tumor metastasis.
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Zhang et al. (2022) studied Platelet activation and aggregation. Momordica charantia exosomes (MCEs) was evaluated on Platelet activation, adhesion, and aggregation. Momordica charantia exosomes at 200 μg/ml exerted the most pronounced inhibitory effect on platelet activation, adhesion, and aggregation, and significantly reduced in vivo thrombus agglutination.
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