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. 2021 Nov 10;8:762363. doi: 10.3389/fnut.2021.762363

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Copyright © 2021 Lin, Chen, Chen, Lin, Wu, Juan and Chang.

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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GlcN stimulates the activation of STAT3 and ERK1/2 in MDSCs. The level and mean fluorescence intensity (MFI) of (A) phosphorylated STAT3 (pSTAT3) and (B) phosphorylated ERK1/2 (pERK1/2) in BM CD11b⁺Gr1⁺, CD11b⁺Gr1⁻, and CD11b⁻Gr1⁻ cells were shown. (C) The levels of phospho-STAT3, STAT3, phospho-ERK1/2 and ERK1/2 in GlcN-treated CD11b⁺ cells were detected by Western analysis. (D) JAK2 inhibitor AG490 and (E) MEK inhibitor PD98059 were used to suppress GlcN-induced phosphorylation of STAT3 and ERK1/2 proteins, respectively, in BM CD11b⁺Gr1⁺ cells. (F) Inhibition of either STAT3 or ERK1/2 decreased GlcN-promoted ROS production in CD11b⁺Gr1⁺ MDSCs. Quantified results are presented as the mean ± standard deviation. *P < 0.05; **P < 0.01; ***P < 0.001.