Conclusion
These data exhibit that alpha-mangostin, comparable to metformin, protects endothelial cells against metabolic memory-induced senescence, which is likely via SIRT1.
Methods
To induce the memory senescence model, HUVECs, after three days incubation with high glucose, were incubated with normal glucose for another three days, and for whole six days, cells were treated with metformin (50 µM) or alpha-mangostin (1.25 µM). On the last day, cell viability by MTT assay, oxidative stress by fluorimetric assay, the number of senescent cells by SA beta-galactosidase staining kit, and secretory interleukin-6 by ELISA kit were measured. SIRT1 and P53 proteins were also evaluated by Western blotting.
Results
Metformin and alpha-mangostin significantly increased cell viability, decreased reactive oxygen species, and senescence-associated beta-galactosidase in HUVECs incubated in metabolic memory condition. Generally, metabolic memory increased p53 and acetyl-P53 and decreased SIRT1 proteins in HUVECs, which were reversed by alpha-mangostin and metformin.