AMD3465 (hexahydrobromide) rescues the MG63 osteoblasts against the apoptosis induced by high glucose - 16/04/21
páginas | 6 |
Iconografías | 4 |
Vídeos | 0 |
Otros | 0 |
Abstract |
Diabetic osteoporosis (DOP) is a serious complication of diabetes, which brings a heavy burden to patients' families and society. The SDF-1/CXCR4 signal pathway may be a target to prevent articular cartilage degeneration. In this study, we studied the effects of high glucose (20 mmol/L) and CXCR4 antagonist AMD3465 (10 μmol/L) on the apoptosis and gene expression of osteoblast-like cells MG63 to determine a new treatment for DOP. CCK8 and clone formation assays confirmed that AMD3465 resisted the decrease of proliferation caused by high glucose. According to the results of scratch and transwell analysis, AMD3465 could remedy the decrease of cell migration and invasion induced by high glucose. The results of flow cytometry analysis and double staining with Hoechst and PI showed AMD3465 corrected the apoptosis induced by high glucose. In addition, high glucose regulated the expression of cell cycle- and apoptosis-related proteins, while AMD3465 blocked the regulation of high glucose. Furthermore, high glucose enhanced the expression levels of SDF-1 and CXCR4 in MG63 cells, as well as the release of MMP1, 3, 9 and 13. AMD3465 inhibited the release of MMPs. The results showed that AMD3465 resisted the apoptosis of MG63 cells induced by high glucose, provided a new strategy for the therapy of DOP.
El texto completo de este artículo está disponible en PDF.Highlights |
• | AMD3465 on MG63 cells apoptosis. |
• | AMD3465 on MMPs release. |
• | A new treatment for DOP. |
Keywords : AMD3465, Diabetic osteoporosis, MG63 cell, Apoptosis, CXCR4
Esquema
Vol 138
Artículo 111476- juin 2021 Regresar al númeroBienvenido a EM-consulte, la referencia de los profesionales de la salud.
El acceso al texto completo de este artículo requiere una suscripción.
Bienvenido a EM-consulte, la referencia de los profesionales de la salud.
La compra de artículos no está disponible en este momento.
¿Ya suscrito a @@106933@@ revista ?