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

Inflammation

Department of General Surgery, The Fourth Hospital of Harbin Medical University, Harbin, Heilongjiang Province, 150001, People's Republic of China.

Published: December 2014

AI Article Synopsis

  • PPAR-γ is a nuclear receptor that regulates lipid metabolism and inflammation, and this study investigates the effects of the synthetic agonist rosiglitazone on LPS-induced mastitis in rats.
  • Rosiglitazone was administered before LPS injection, showing a reduction in inflammatory cell infiltration and decreased levels of inflammatory markers like TNF-α and IL-6.
  • The study concludes that rosiglitazone protects against mastitis by inhibiting NF-κB signaling pathways, suggesting that PPAR-γ could be a potential therapeutic target for this condition.

Article Abstract

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.

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http://dx.doi.org/10.1007/s10753-014-9924-zDOI Listing

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