Figure 6.

Inhibition of microglia activation by PPARβ/δ was associated with repression of NF-κB and MAPK activities. (a) Primary microglia were treated with vehicle or BA for 12 h. Cells were then stimulated with or without LPS (100 ng/ml) for 3 h. Levels of PPARβ/δ mRNA were analyzed by real-time PCR. Data are normalized to the gene expression in vehicle-treated microglia without LPS stimulation and shown as mean±S.E.M. (n=6). (b) Top, BV2 cells were transfected with control (Ctrl) siRNA or PPARβ/δ siRNA (siPPARβ/δ) and cultured for 24 h, then subjected to immunoblot analyses of PPARβ/δ. Middle and bottom, BV2 cells were transfected with control (Ctrl) siRNA or PPARβ/δ siRNA. Cells were pre-treated with vehicle or BA (20 μM) for 12 h, and then cultured in the absence or presence of LPS for 3 h. Expression of proinflammatory cytokines and chemokines were analyzed by real-time PCR. Data are normalized to the gene expression in vehicle-treated VB2 cells without LPS stimulation and shown as mean±S.E.M. (n=6). (c) BV2 cells were pre-treated with vehicle or BA (10 or 20 μM) for 12 h, and then cultured in the absence or presence of LPS for 10 or 30 min. Levels of IκBα, p-IκBα, p38, p-p38, JNK, p-JNK, ERK and p-ERK were determined by immunoblot analyses. Results in b (top) and c are representative of three independent experiments with similar results. *P<0.05; **P<0.01