Open Access

Rosiglitazone alleviates lipopolysaccharide‑induced inflammation in RAW264.7 cells via inhibition of NF‑κB and in a PPARγ‑dependent manner

  • Authors:
    • Jing-Ping Zhou
    • Xiao-Ning Yang
    • Yang Song
    • Fei Zhou
    • Jing-Jing Liu
    • Yi-Qun Hu
    • Li-Gang Chen
  • View Affiliations

  • Published online on: May 11, 2021     https://doi.org/10.3892/etm.2021.10175
  • Article Number: 743
  • Copyright: © Zhou et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

Rosiglitazone is a synthetic peroxisome proliferator‑activated receptor (PPAR)γ agonist widely used for the treatment of type 2 diabetes. Recent studies have demonstrated that rosiglitazone displays anti‑inflammatory effects. The present study aimed to investigate whether rosiglitazone alleviates decreases in RAW264.7 cell viability resulting from lipopolysaccharide (LPS)‑induced inflammation, as well as exploring the underlying mechanism. A macrophage inflammatory injury model was established by treating RAW264.7 cells with 100 ng/ml LPS. Cells were divided into LPS and rosiglitazone groups with different concentrations. Cell viability was assessed by performing an MTT assay. The expression of inflammatory cytokines was detected by conducting enzyme‑linked immunosorbent assays and reverse transcription‑quantitative PCR. Nitric oxidesecretion was assessed using the Griess reagent system. The expression levels of key nuclear factor‑κB pathway‑associated proteins were detected via western blotting. Rosiglitazone alleviated LPS‑induced decrease in RAW264.7 cell viability and inhibited inflammatory cytokine expression in a concentration‑dependent manner. Rosiglitazone significantly inhibited LPS‑induced upregulation of p65 phosphorylation levels and downregulated IκBα expression levels. However, rosiglitazone‑mediated inhibitory effects were reversed by PPARγ knockdown. The results of the present study demonstrated that rosiglitazone significantly inhibited LPS‑induced inflammatory responses in RAW264.7 macrophage cells, which was dependent on PPARγ activation and NF‑κB suppression.
View Figures
View References

Related Articles

Journal Cover

July-2021
Volume 22 Issue 1

Print ISSN: 1792-0981
Online ISSN:1792-1015

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Zhou J, Yang X, Song Y, Zhou F, Liu J, Hu Y and Chen L: Rosiglitazone alleviates lipopolysaccharide‑induced inflammation in RAW264.7 cells via inhibition of NF‑κB and in a PPARγ‑dependent manner. Exp Ther Med 22: 743, 2021
APA
Zhou, J., Yang, X., Song, Y., Zhou, F., Liu, J., Hu, Y., & Chen, L. (2021). Rosiglitazone alleviates lipopolysaccharide‑induced inflammation in RAW264.7 cells via inhibition of NF‑κB and in a PPARγ‑dependent manner. Experimental and Therapeutic Medicine, 22, 743. https://doi.org/10.3892/etm.2021.10175
MLA
Zhou, J., Yang, X., Song, Y., Zhou, F., Liu, J., Hu, Y., Chen, L."Rosiglitazone alleviates lipopolysaccharide‑induced inflammation in RAW264.7 cells via inhibition of NF‑κB and in a PPARγ‑dependent manner". Experimental and Therapeutic Medicine 22.1 (2021): 743.
Chicago
Zhou, J., Yang, X., Song, Y., Zhou, F., Liu, J., Hu, Y., Chen, L."Rosiglitazone alleviates lipopolysaccharide‑induced inflammation in RAW264.7 cells via inhibition of NF‑κB and in a PPARγ‑dependent manner". Experimental and Therapeutic Medicine 22, no. 1 (2021): 743. https://doi.org/10.3892/etm.2021.10175