Figure 5.

PNPLA3 mediated the NF‐kB regulation of inflammation in PA‐treated HepG2 cells. A, PNPLA3 mediated NF‐kB regulation of TNF‐α expression in HepG2 cells. HepG2 cells were transfected with pCMV‐p65, or cotransfected with pCMV‐p65 and siRNA‐PNPLA3. Cells transfected with the pCMV‐Mock or/and siRNA‐Mock were used as negative control. Cell lysates were collected 24 h post‐transfection. The protein expressions of NF‐kB, PNPLA3 and TNF‐α were detected by Western blotting. B, Inhibition of PNPLA3 alleviated PA‐induced hepatocyte inflammation. HepG2 cells were treated with PA for 24 h with pre‐transfection of siRNA‐Mock or siRNA‐PNPLA3. The mRNA levels of PNPLA3 and TNF‐α were detected by real‐time PCR. The results are presented as the mean ± SD from three independent experiments. #P < .05 compared with siRNA‐Mock‐transfected cells, *P < .05 compared with siRNA‐Mock‐transfected cells treated with BSA; C, Overexpression of PNPLA3 M148M prevented NF‐kB inhibitor‐induced reduction of PA‐related inflammation. HepG2 cells that stably transfected with LV‐148M or LV‐Mock were treated with PA for 24 h with or without pretreatment of BAY‐117082. Cell lysates were harvested to measure the protein expressions of PNPLA3 and TNF‐α by Western blotting