Inhibitory effect of zinc on the advanced glycation end product-induced apoptosis of mouse osteoblastic cells

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E-ISSN： 1791-3004|12|4|5286-5292

ISSN： 1791-2997

Source： Molecular Medicine Reports, Vol.12, Iss.4, 2015-01, pp. : 5286-5292

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Abstract

Osteoporosis and diabetes have become serious health problems worldwide. Previous studies have suggested that diabetes is associated with osteoporosis and increased fracture risk. However, the mechanism underlying diabetesinduced osteoporosis remains to be elucidated. Therefore, the present study aimed to examine the mechanism underlying diabetesinduced osteoporosis, and determine the protective effects of zinc, which is known to be closely associated with osteoporosis and diabetes. The results of the present study demonstrated that zinc inhibited advanced glycation end product (AGE)induced MC3T3E1 cell apoptosis by attenuating the production of reactive oxygen species, inhibiting caspase3 and caspase9 activation, and inhibiting the release of cytochrome c from between the mitochondria and the cytosol. Furthermore, zinc was found to protect cells against AGEinduced apoptosis via the mitogenactivated protein kinase/extracellular signalregulated kinase and phosphoinositide 3kinase/AKT signaling pathways. In conclusion, these findings enable a better understanding of the mechanism underlying diabetesinduced osteoporosis, and may indicate a novel target for its prevention and treatment.