SREBP1 Antibody - #AF4728

Figure 3. PCA promotes fatty acid metabolism through SIRT3 activation. (A-E) Western blotting and real-time PCR analysis of hepatic FASN, SREBP-1c, CPT1, Acox1 and PPARα protein (n=5) and mRNA (n=6) levels in mouse livers. *P< 0.05 vs. the WT ND group, #P< 0.05 vs. the WT HFD group, &P< 0.05 vs. the SIRT3−/− ND group. (F-I) The protein expression of FASN, SREBP-1c, CPT1, Acox1, PPARα and SIRT3 was measured by Western blotting (n=5). The mRNA levels of (J) FASN, SREBP-1c (K) CPT1, Acox1 and PPARα were measured with real-time PCR (n=6). *P< 0.05 vs. the si-Control group, #P< 0.05 vs. the si-Control+PA group, &P< 0.05 vs. the si-Control+PA+PCA group.

Figure 3. Effects of AMC on the protein levels of AMPKα-SREBP-1c/PPARα-regulating hepatic lipid metabolism in transported rats. (A–D) The protein levels of phosphorylated AMP-activated protein kinase alpha (p-AMPKα)/AMPKα, AMP-activated protein kinase alpha (AMPKα), AMPKα1, AMPKα2, sterol regulatory element-binding protein-1c (SREBP-1c), and Peroxisome proliferator-activated receptor alpha (PPARα) in the liver (A) on days −3 and 0, (B) at IAT, (C) on day 3, and (D) on day 10. Rats were assigned to one of six groups: Con, TS, ABT, VBT, AAT, and VAT groups. Data are expressed as the mean ± standard error of the mean (n = 6). * mean Con group on day −3 vs. day 0; Con vs. ABT or VBT on day 0; TS vs. Con, ABT, or VBT at IAT; and TS vs. Con, ABT, VBT, AAT, or VAT on days 3 and 10; # (black) mean ABT vs. VBT on days 0, 3, and 10 and at IAT, and AAT vs. VAT on days 3 and 10; # (red) mean ABT vs. AAT and VBT vs. VAT on days 3 and 10. *, # (black), and # (red): p < 0.05; **, ## (black), and ## (red): p < 0.01.

Fig. 2. Siah1 overexpression exacerbates HFD-induced lipid accumulation. A. Biochemical markers of liver function in the serum of Ad-Siah1 and Ad-GFP mice fed with 60% HFD for 16 weeks. B. Representative images of macroscopic examination, HE (original magnification, ×100) and oil red O (original magnification, ×400) staining of mice liver tissue obtained from Ad-Siah1 and Ad-GFP mice fed with 60% HFD for 16 weeks. C. Changes in liver weights. D. Spectrometer quantification of oil red O staining. E-F. Relative protein and mRNA expression levels of Siah1 and lipid metabolic genes (SREBP1, FASN and ACC1) in mice liver tissue obtained from Ad-Siah1 and Ad-GFP mice fed with 60% HFD for 16 weeks. G-H. Lipid accumulations displayed by oil red O staining (original magnification, ×200) and spectrometer quantification in Hepa1-6/Ad-Siah1 or AML12/Ad-Siah1 cells after 24 h OA/PA treatment. I-J. Relative protein and mRNA expression levels of Siah1 and lipid metabolic genes (SREBP1, FASN and ACC1) in Hepa1-6/Ad-Siah1 or (K-L) AML12/Ad-Siah1 cells after 24 h OA/PA treatment. The data are presented as mean ± SD. Student’s t-test was used to evaluate the statistical significance. *P < 0.05, **P < 0.01 vs. Ad-GFP.

Figure 5 Effects of Si-Ni-San (SNS) on the protein expressions related to lipid metabolism. The protein expressions of FAS, CPT-1, nuclear and cytosolic SREBP-1c and PPARα were determined by Western blot. (A and B) Typical bands of Western blot, (C–F) gray value of Western blot bands. The data are stated as the means ± SD. n = 3 *vs CON group (P < 0.05), #vs MOD group (P < 0.05). Liver was obtained from control group (CON), model group (MOD), low-dose SNS group (SNS-L), high-dose SNS group (SNS-H), and metformin group (MET).

Figure 7 The expression levels of lipid metabolism-related proteins after chronic lactate and forskolin injection. (A) Western blot analysis and relative fold protein expression of lipolysis-related proteins. (B) Western blot analysis and relative fold protein expression of lipogenesis-related proteins. CP, chronic PBS treated group; CL, chronic lactate treated group; CF, chronic forskolin treated group; CD, chronic DMSO treated group; and CLF, chronic lactate and forskolin treated group. Relative expression levels were normalized to GAPDH. Three bands are used for statistics. The data are presented as the mean±SD, and significant differences among the groups were analyzed with one-way ANOVA. * p<0.05.

Fig. 2 Validation of the predicted genes in ox-LDL-induced mouse macrophages. A, circSnd1, miR-485-3p, and Olr1 mRNA expression verification. B, Olr1 protein expression verification. C, Verification of the expression changes in inflammatory signaling molecules possibly downstream of the circSnd1/miR-485-3p/Olr1 axis in mouse macrophages after treatment with ox-LDL. D, Changes in the expression of key proteins in lipid metabolism in ox-LDL-induced mouse macrophages. *, #p < 0.05; **, ##p < 0.01.

Fig. 1 Effect of taurine on the TG level and FA synthesis-related enzymes and factors protein level in HepG2 cells. (a) TG levels; (b, d) protein band diagram; (c, e) Relative protein level. C: control group; CT: control supplemented with taurine; M: steatotic cell model; MT: steatotic model supplemented with taurine. ∗p < 0.05 vs. C group; #p < 0.05 vs. M group.

Fig. 3. Effects of EGCG on the expressions of the key enzymes and transcription factor of fatty acid de novo synthesis in HCT116 cells. (A) The expressions of ACLY, FASN, ACC, SCD1, and SREBP1c at the mRNA level as determined using qRT-PCR. (B-C) Western blot and densitometry analysis. The relative intensities of proteins were calculated after normalization to β-Actin. (D-E) Immunofluorescence staining and quantification of FASN, scale bar: 20 μm. Data represent the means ± SE from three independent experiments (A and C) or from three independent experiments with 2 duplicates (E). Statistical analysis was performed using one-way ANOVA with post hoc Bonferroni’s correction test. Groups containing different lowercase letters (a-e) indicate statistical significance at the level of p < 0.05.