Open Access

Protective effects of budesonide on LPS‑induced podocyte injury by modulating macrophage M1/M2 polarization: Evidence from in vitro and in silico studies

  • Authors:
    • Xilan Zhang
    • Guangying Wang
    • Dayue Shen
    • Yating Feng
    • Yan Zhang
    • Chao Zhang
    • Yuanping Li
    • Hui Liao
  • View Affiliations

  • Published online on: July 26, 2022     https://doi.org/10.3892/etm.2022.11526
  • Article Number: 589
  • Copyright: © Zhang 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

Budesonide (Bud), one of the most widely used lung medicines, is currently used as a repurposing medicine for immunoglobulin A nephropathy (IgAN) treatment. The progression of IgAN is related to inflammation involving macrophages and podocytes. The present study aimed to explore the effects of Bud on classically activated (M1)/alternatively activated (M2) macrophage polarization and podocyte injury under lipopolysaccharide (LPS)‑induced inflammatory stress in vitro. Anti‑inflammatory bioinformation of Bud was identified based on the Gene Expression Omnibus database. RAW264.7 cells were treated with normal medium, LPS, curcumin (Cur, positive control), or Bud 5, 10, or 20 µM. The expression levels of inducible nitric oxide synthase (iNOS), TNF‑α, mannose receptor (CD206) and arginase (Arg)‑1 were quantified by western blotting. The collected supernatants from macrophages were termed (Nor)MS, (LPS)MS, (Cur)MS and (Bud)MS. The TNF‑α, IL‑1β and nitric oxide (NO) levels in the supernatants were evaluated by ELISA and Griess assay. The podocytes were cultured in different supernatants and their survival rates were assessed by bromodeoxyuridine assay. TNF signaling is an important pathway by which Bud exerts anti‑inflammatory activities. Compared with the LPS group, 5, 10 and 20 µM Bud significantly increased Arg‑1 and decreased iNOS expression (Six: P<0.05) and 20 µM Bud significantly increased Arg‑1 and CD206 and decreased iNOS and TNF‑α expression (Four: P<0.05). Cur significantly decreased iNOS and TNF‑α expression (Two: P<0.05). Compared with LPS, 5, 10 and 20 µM Bud and Cur significantly decreased TNF‑α, IL‑1β and NO levels (All: P<0.05). The podocyte survival rates of (Bud)MS and (Cur)MS were significantly higher than those of (LPS)MS (Four: P<0.05). The protective effect of Bud on podocyte injury is related to its modulation of M1/M2 polarization.
View Figures
View References

Related Articles

Journal Cover

September-2022
Volume 24 Issue 3

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
Zhang X, Wang G, Shen D, Feng Y, Zhang Y, Zhang C, Li Y and Liao H: Protective effects of budesonide on LPS‑induced podocyte injury by modulating macrophage M1/M2 polarization: Evidence from <em>in vitro</em> and <em>in silico</em> studies. Exp Ther Med 24: 589, 2022
APA
Zhang, X., Wang, G., Shen, D., Feng, Y., Zhang, Y., Zhang, C. ... Liao, H. (2022). Protective effects of budesonide on LPS‑induced podocyte injury by modulating macrophage M1/M2 polarization: Evidence from <em>in vitro</em> and <em>in silico</em> studies. Experimental and Therapeutic Medicine, 24, 589. https://doi.org/10.3892/etm.2022.11526
MLA
Zhang, X., Wang, G., Shen, D., Feng, Y., Zhang, Y., Zhang, C., Li, Y., Liao, H."Protective effects of budesonide on LPS‑induced podocyte injury by modulating macrophage M1/M2 polarization: Evidence from <em>in vitro</em> and <em>in silico</em> studies". Experimental and Therapeutic Medicine 24.3 (2022): 589.
Chicago
Zhang, X., Wang, G., Shen, D., Feng, Y., Zhang, Y., Zhang, C., Li, Y., Liao, H."Protective effects of budesonide on LPS‑induced podocyte injury by modulating macrophage M1/M2 polarization: Evidence from <em>in vitro</em> and <em>in silico</em> studies". Experimental and Therapeutic Medicine 24, no. 3 (2022): 589. https://doi.org/10.3892/etm.2022.11526