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. 2015 May 1;10(5):e0124951. doi: 10.1371/journal.pone.0124951

Fig 2. AICAR-activated AMPK decreased SREBP-2 protein levels.

Fig 2

(A) HepG2 cells were treated with or without 0.5 mmol/l (0.5 mM) AICAR for 12 or 24 h and were subsequently washed with phosphate-buffered saline (PBS) and lysed. Nuclear and cytoplasmic extracts were analyzed by WB. β-actin was used as a cytoplasmic marker, and LaminB1 (LMNB1) was used as the nuclear marker. (B-C) Densitometric quantification of SREBP-2 (P) and SREBP-2 (N). The data are presented as the mean ± SEM. *p< 0.05 versus control (con, without AICAR). (D) AICAR-activated AMPK inhibited the expression of SREBP-2 in HepG2 cells. HepG2 cells were treated with or without 0.5 mM AICAR for 12 or 24 h and then were harvested to determine the mRNA expression of SREBP-2. β-actin was used for normalization, and the control was set to 1 in the Real-Time PCR data. All the experiments were performed in duplicate. *p < 0.05 versus control. (E) Immunofluoresence images of SREBP-2 (red) and nuclear staining with 4', 6-diamidino-2-phenylindole (DAPI, blue) in HepG2 cells. Magnification, ×200. Semiquantification analysis by ImageJ software of fluorescence intensity of SREBP-2 precusor and nuclear form in HepG2 cells. Bar-graph represents the results from 3 separate experiments and the fluorescence intensity of SREBP-2 from HepG2 cells without AICAR treatment was set as 1.