Cell Biology Int. (2009) Immediate Publication

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Cell Biology International (2009) Immediate Publication, doi:10.1042/CBI20090005

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Pioglitazone suppresses the lipopolysaccharide-induced production of inflammatory factors in mouse macrophages by inactivating NF-κB

Caihui Ao, Yong Huo, Litong Qi, Zhuowei Xiong, Lin Xue and Yongfen Qi

Department of Cardiology, Peking University First Hospital, Beijing, China. huoyong@263.net.cn

Thiazolidinediones (TZDs) are prescribed as anti-type II diabetes drugs, but little is known regarding whether TZDs regulate the expression of secretory phospholipase A2 (sPLA2) in macrophage. We have investigated the effects of pioglitazone on LPS-induced production of tumor necrosis factor alpha (TNF-α), group V and X sPLA2(sPLA2-V and -X) in RAW 264.7 macrophage. TNF-α, sPLA2-V and sPLA2-X mRNA and protein expression was determined by RT-PCR and Western blot analysis, respectively. The activity of nuclear factor κB (NF-κB) was determined by Western blot and confocal microscopy. LPS induced TNF-α, sPLA2-V and sPLA2-X mRNA and protein expression. Pretreatment with 10 μmol/L pioglitazone significantly suppressed LPS-induced TNF-α, sPLA2-V and sPLA2-X mRNA and protein expression. LPS induced NF-κB expression and translocation in the nucleus, but the inductive effects was inhibited by pioglitazone. Our findings indicate that pioglitazone inhibits production of inflammatory factors induced by LPS in murine macrophage cells by inactivating NF-kB. Pioglitazone appears to play an anti-inflammatory role in atherosclerosis process.

doi:10.1042/CBI20090005
Received 25 September 2008/5 July 2009; Accepted 9 September 2009
Published as Immediate Publication 9 September 2009