In this task, you are given an abstract of article. Your task is to generate title for this article. Preferred titles are under thirty words.
Q: OBJECTIVE Advances made in the past ten years highlight the notion that peroxisome proliferator-activated receptors gamma (PPAR) has protective properties in the pathophysiology of osteoarthritis (OA). The aim of this study was to define the roles of PPAR in AGEs-induced inflammatory response in human chondrocytes.
METHODS Primary human chondrocytes were stimulated with AGEs in the presence or absence of neutralizing antibody against RAGE (anti-RAGE), MAPK specific inhibitors and PPAR agonist pioglitazone. The expression of IL-1, MMP-13, TNF-, PPAR, nuclear NF-B p65 and cytosol IB was determined by western blotting and real-time PCR.
RESULTS AGEs could enhance the expression of IL-1, TNF-, and MMP-13, but the level of PPAR was decreased in a time- and dose-dependent manner, which was inhibited by anti-RAGE, SB203580 (P38 MAPK specific inhibitor) and SP600125 (a selective inhibitor of JNK). PPAR agonist pioglitazone could inhibit the effects of AGEs-induced inflammatory response and PPAR down-regulation. In human chondrocytes, AGEs could induce cytosol IB degradation and increase the level of nuclear NF-B p65, which was inhibited by PPAR agonist pioglitazone.
CONCLUSIONS In primary human chondrocytes, AGEs could down-regulate PPAR expression and increase the inflammatory mediators, which could be reversed by PPAR agonist pioglitazone. Activation of RAGE by AGEs triggers a cascade of downstream signaling, including MAPK JNK/ p38, PPAR and NF-B. Taken together, PPAR could be a potential target for pharmacologic intervention in the treatment of OA.
A:
The Role of PPAR in Advanced Glycation End Products-Induced Inflammatory Response in Human Chondrocytes