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. 2017 Mar 7;11:64. doi: 10.3389/fncel.2017.00064

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Copyright © 2017 Song, Choi and Kim.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution and reproduction in other forums is permitted, provided the original author(s) or licensor 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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The change in PPAR-γ signaling by inhibiting AdipoR1 in Aβ-treated BV2 microglia. The protein levels of CD86 (A) and p-NF-κB (B) p-PPAR-γ (C) protein were detected by western blotting analysis. (C) The decreased p-PPAR-γ protein level by Acrp30 and GW9662 in Aβ-treated microglia was not changed by suppressing AdipoR1. Data are expressed as mean ± SEM. Each experiment was conducted four times per condition. GAPDH served as a control. Differences were considered statistically significant at *p < 0.05 (compared to control). Acrp30: Acrp30 5 μg/ml pretreatment, Aβ: Aβ 10 μM treatment for 24 h, siAdipoR1: siRNA AdipoR1 transfection, GW9662: PPAR-γ antagonist 10 μM. **p < 0.001.