Effects of PPAR-γ agonist treatment on LPS-induced mastitis in rats

Inflammation. 2014 Dec;37(6):1919-24. doi: 10.1007/s10753-014-9924-z.


PPAR-γ, a member of the nuclear receptor superfamily, plays an important role in lipid metabolism and inflammation. The aim of this study was to investigate the preventive effects of synthetic PPAR-γ agonist rosiglitazone on lipopolysaccharide (LPS)-induced mastitis in rats. The mouse model of mastitis was induced by the injection of LPS through the duct of the mammary gland. Rosiglitazone was injected 1 h before the induction of LPS intraperitoneally. The results showed that rosiglitazone attenuated the infiltration of inflammatory cells, the activity of myeloperoxidase (MPO), and the production of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β) in a dose-dependent manner. Additionally, Western blotting showed that rosiglitazone inhibited the phosphorylation of IκB-α and NF-κB p65. These results indicated that rosiglitazone has a protective effect on mastitis, and the anti-inflammatory mechanism of rosiglitazone on LPS-induced mastitis in rats may be due to its ability to inhibit NF-κB signaling pathways. PPAR-γ may be a potential therapeutic target against mastitis.

MeSH terms

  • Animals
  • Dose-Response Relationship, Drug
  • Female
  • Lipopolysaccharides / toxicity*
  • Mastitis / chemically induced*
  • Mastitis / metabolism
  • Mastitis / prevention & control*
  • PPAR gamma / agonists*
  • PPAR gamma / metabolism
  • Pregnancy
  • Random Allocation
  • Rats
  • Rats, Sprague-Dawley
  • Rosiglitazone
  • Thiazolidinediones / pharmacology
  • Thiazolidinediones / therapeutic use*


  • Lipopolysaccharides
  • PPAR gamma
  • Thiazolidinediones
  • Rosiglitazone