Peroxisome Proliferator-Activated Receptor- Prevents Cholesterol Gallstone Formation in C57bl Mice by Regulating Bile Acid Synthesis and Enterohepatic Circulation

Figure 6

PPARγ regulates genes involved in EHC in LO2 and Caco2 cell lines by FXR dependent mechanisms. LO2 cells were stably transfected with PPARγ overexpression (L02pre) or negative control vector (L02NC). (a) mRNA expression of PPARγ, LXRα, LXRβ, FXR, BSEP, ABCB4, CYP7A1, CYP27A1, MRP2, and MRP4 in PPARγ-overexpressed L02 cells, as determined by real-time RT-PCR. L02pre were further transfected with FXR siRNA. (b) mRNA expression of FXR, BSEP, and MRP2 was determined by real-time RT-PCR. GAPDH was used for data normalizing. Western blotting was performed on BSEP. (c) 10μM pioglitazone was used for activation of PPARγ, and siRNA targeting FXR was used for downregulating FXR. mRNA expression of FXR, OSTα, and ASBT was determined by real-time RT-PCR. (d) Western blotting was performed on ASBT and OSTα in Caco2 cell treated as previously established. Data are presented as the means ± SEM of three independent experiments performed in duplicate. P<0.05, P<0.01, and #P>0.05.

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