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Copyright (c) 2023 Itandehui Belem Gallegos-Velasco, Miguel Ángel Pérez-Acevedo, Berenice Fernández-Rojas, Pedro Antonio Hernández-Cruz, Jesús Hernández-Juárez
This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.
The undersigned hereby assign all rights, included but not limited to copyright, for this manuscript to CMB Association upon its submission for consideration to publication on Cellular and Molecular Biology. The rights assigned include, but are not limited to, the sole and exclusive rights to license, sell, subsequently assign, derive, distribute, display and reproduce this manuscript, in whole or in part, in any format, electronic or otherwise, including those in existence at the time this agreement was signed. The authors hereby warrant that they have not granted or assigned, and shall not grant or assign, the aforementioned rights to any other person, firm, organization, or other entity. All rights are automatically restored to authors if this manuscript is not accepted for publication.Glucosamine effects on platelet aggregation of type 2 diabetes mellitus patients: in vitro assays
Corresponding Author(s) : Hernández-Juárez Jesús
Cellular and Molecular Biology,
Vol. 69 No. 4: Issue 4
Abstract
Hyperglycemia, insulin resistance, and endothelium dysfunction are related to platelet hyperactivity in type 2 diabetes mellitus (T2D) patients. Glucosamine (GlcN) has inhibitory effects on platelets of animals and healthy donors, but this role in platelets from T2D patients is unknown. The aim of this study was to evaluate the GlcN in vitro effects on platelet aggregation in T2D patients and healthy donors. Donors´ and T2D patients' samples were analyzed through flow cytometry, Western blot, and platelet aggregometry. Platelet aggregation was induced using ADP and thrombin, with or without GlcN, N-Acetyl-glucosamine, galactose, or fucose. GlcN inhibited ADP and thrombin-induced platelet aggregation, while the other carbohydrates did not. GlcN suppressed the second wave of ADP-induced platelet aggregation. No differences in the percent of inhibition of ADP-induced platelet aggregation by GlcN were found between donors and T2D patients, but this effect was significantly higher in healthy donors using thrombin as an agonist. In addition, GlcN increased protein O-GlcNAcylation (O-GlcNAc) in the platelets from T2D patients but not in healthy donors. In conclusion, GlcN inhibited the platelet aggregation induced by ADP and thrombin for both study groups and increased O-GlcNAc in platelets from T2D patients. Further studies are required to evaluate the possible use of GlcN as an antiplatelet agent.
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