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. 2022 Mar 7;13:817596. doi: 10.3389/fphar.2022.817596

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Copyright © 2022 Yuan, Hu, Liu, Xie, Yang, Li, Zhang, Chen, Tang and Shen.

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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DCL suppresses LPS/IFNγ-induced inflammatory response in murine macrophages. (A) Cell viability of LPS/IFNγ-stimulated RAW264.7 cells treated with different concentrations of DCL or BAY was measured by CCK-8 assay. (B) The effects of DCL on NO production in LPS (0.5 μg/ml)/IFNγ (10 ng/ml)-stimulated murine RAW264.7 macrophage cell line and murine primary PMs. (C) The effect of DCL on LPS/IFNγ-induced PGE₂ release in RAW264.7 cells. (D) Western blot analysis of iNOS and COX-2 from RAW264.7 cells subjected to LPS/IFNγ stimulation and treated with different concentrations of DCL or BAY. The densitometry analysis of iNOS (E) and COX-2 (F), normalized against β-Actin. Data are represented as mean ± SEM, n = 3. ^# p < 0.05, ^## p < 0.01, ^### p < 0.001, ^#### p < 0.0001 compared to the control check (CK) group. ^* p < 0.05, ^** p < 0.01, ^*** p < 0.001, ^**** p < 0.0001 compared to LPS/IFNγ group.