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. 2018 May 9;9:447. doi: 10.3389/fphar.2018.00447

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Copyright © 2018 Liu, Yang, Mu and Fu.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Effect of EGCG on DEX-induced osteoblast cellular dysfunction. (A) EGCG improved cell viability, increased ALP activity, and recovered SOD expression in primary osteoblasts treated with DEX. (B) EGCG reversed cellular and mitochondrial oxidative stress according to cytometry of DCFH-DA and mitoSOX staining. (C) Expression of Nrf2 and downstream transcriptional factor HO-1 during EGCG protection under high-dose DEX treatment. Protein levels were statistically evaluated in columns. Measurements were in triplicate and data are presented as the mean ±SD. ^##P < 0.01, ^#P < 0.05 vs. control; ^∗∗P < 0.01, ^∗P < 0.05 vs. DEX; and ^ΦP < 0.05 DEX+EGCG vs. control.