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Published:
Mar 6, 2018DOI:
10.4314/tjpr.v17i2.2Keywords:
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Main Article Content
Calycosin regulates glucocorticoid-induced apoptosis via Nrf2/ARE signaling in MC3T3-E1 cells
Abstract
Purpose: To determine the anti-osteoporotic effect of calycosin (CA) and investigate the mechanism involved.
Methods: To establish a cell model of osteoporosis, MC3T3-E1 cells were treated with dexamethasone (DEX). Subsequently, the levels of accumulated reactive oxygen species (ROS) and subsequent apoptotic cell death (using flow cytometry) were determined. Relevant mRNA and protein expression levels were measured by quantitative reverse transcription polymerase chain reaction (qRT-PCR) and immunoblot respectively.
Results: CA reduced the apoptosis and accumulation of ROS in DEX-treated cells. DEX induced the expression of caspase-3/-8/-9 in the cleavage of poly ADP-ribose polymerase (PARP), whereas CA treatment decreased expression levels of caspase-3/-8/-9 and PARP. In addition, DEX treatment significantly suppressed the expression of nuclear factor-erythroid 2-related factor 2 (Nrf2) as well as its downstream targets, viz, heme oxygenase-1 and quinone oxidoreductase-1. Interestingly, CA treatment reversed this suppressive effect. It was also found that Nrf2 small interfering RNA effectively inhibited the protective effects of CA against DEX-induced ROS overproduction as well as apoptosis.
Conclusion: CA attenuates the cytotoxicity of DEX via inhibition of the generation of ROS and promotion of Nrf2 expression. These findings offer novel insights into a molecular approach to the treatment of glucocorticoid-induced osteoporosis via the application of natural compounds.
Keywords: Calycosin, Osteoporosis, Nrf2, Antioxidant response elements, Apoptosis
