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BioMed Research International
Volume 2014 (2014), Article ID 787924, 14 pages
Research Article

Rosiglitazone Regulates Anti-Inflammation and Growth Inhibition via PTEN

1Institute of Clinical Medicine, National Cheng Kung University Medical College, Tainan 70101, Taiwan
2Department of Medical Laboratory Science and Biotechnology, National Cheng Kung University Medical College, Tainan 70101, Taiwan
3School of Public Health, Taipei Medical University, Taipei 11031, Taiwan
4Department of Life Sciences, College of Bioscience and Biotechnology, National Cheng Kung University Medical College, Tainan 70101, Taiwan
5Department of Nursing, Chung Hwa University of Medical Technology, No. 89, Wen-Hwa 1st Street, Jen-Te Hsiang, Tainan 71703, Taiwan
6Department of Gastroenterology, Shin Kong Wu Ho-Su Memorial Hospital, Taipei 11101, Taiwan

Received 7 June 2013; Revised 18 January 2014; Accepted 1 February 2014; Published 13 March 2014

Academic Editor: Kazim Husain

Copyright © 2014 Chiou-Feng Lin et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Peroxisome proliferator-activated receptor gamma (PPAR) agonist has anti-inflammatory and anticancer properties. However, the mechanisms by which PPAR agonist rosiglitazone interferes with inflammation and cancer via phosphatase and tensin homolog-(PTEN)-dependent pathway remain unclear. We found that lower doses (<25 μM) of rosiglitazone significantly inhibited lipopolysaccharide-(LPS)-induced nitric oxide (NO) release (via inducible nitric oxide synthase, iNOS), prostaglandin E2 (PGE2) production (via cyclooxygenase-2, COX-2), and activation of Akt in RAW 264.7 murine macrophages. However, rosiglitazone did not inhibit the production of reactive oxygen species (ROS). In PTEN knockdown (shPTEN) cells exposed to LPS, rosiglitazone did not inhibit NO release, PGE2 production, and activation of Akt. These cells had elevated basal levels of iNOS, COX-2, and ROS. However, higher doses (25–100 μM) of rosiglitazone, without LPS stimulation, did not block NO release and PGE2 productions, but they inhibited p38 MAPK phosphorylation and blocked ROS generation in shPTEN cells. In addition, rosiglitazone caused G1 arrest and reduced the number of cells in S + G2/M phase, leading to growth inhibition. These results indicate that the anti-inflammatory property of rosiglitazone is related to regulation of PTEN independent of inhibition on ROS production. However, rosiglitazone affected the dependence of PTEN-deficient cell growth on ROS.