15-Deoxy-Δ-Prostaglandin J2 Modulates Lipopolysaccharide-Induced Chemokine Expression by Blocking Nuclear Factor-κB Activation via Peroxisome Proliferator Activated Receptor-γ-Independent Mechanism in Renal Tubular Epithelial Cells.

Conclusion: Collectively, these results suggest that 15d-PGJ2 exerts anti-inflammatory actions on HK-2 cells by attenuating chemokines expression. 15d-PGJ2 inhibits chemokines expression via a PPAR-γ-independent way, which is related to block NF-κB pathway. Since NF-κB is an important regulator of the response of HPTECs to injury, PPAR-γ agonists may represent a key pharmacological target for ameliorating inflammation-associated tubulointerstitial fibrosis. © 2013 S. Karger AG, Basel.
PMID: 23887394 [PubMed - as supplied by publisher]

Source: Nephron Experimental Nephrology - July 24, 2013 Category: Urology & Nephrology Authors: Lu Y, Zhou Q, Zhong F, Guo S, Hao X, Li C, Wang W, Chen N Tags: Nephron Exp Nephrol Source Type: research