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. 2021 Apr 9;12:659597. doi: 10.3389/fphar.2021.659597

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Copyright © 2021 Zhou, Li, Wang, Jiang, Li, Wang, Wang, Ma and Cao.

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(s) 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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Sodium butyrate (NaB) arrests the PI3K/Akt/mTOR signaling pathway in vitro and in vivo. Chondrocytes were pretreated for 2 h with several concentration gradients of NaB and were then stimulated with IL-1β for 24 h (A,B) The protein expression levels of PI3K, p-PI3K, Akt, p-Akt, mTOR, and p-mTOR in chondrocytes were assessed (n = 3). (C) Immunostaining of p-PI3K, p-Akt, and p-mTOR 60 days postoperation and quantification (D–F); scale bar, 100 μm; n = 10 per group. The data are presented as the mean ± S.D. Significant differences between groups were determined by one-way ANOVA; *p < 0.05 and **p < 0.01 vs. IL-1β-induced group or the vehicle group; ^# p < 0.01 vs. control group or the sham group; NS (not significant) vs. control group or the sham group. PI3K, phosphoinositide 3-kinase; Akt, protein kinase B; mTOR, mammalian target of rapamycin; IL-1β, interleukin-1β.