PPAR alpha Antibody - #AF5301

Fig. 6. β-PAE promotes the expression of hepatic lipid oxidation-related proteins and genes in HFD-fed rats. (A–G) Western blot analysis on the expression of SIRT1, PGC-1α, PPARα, FGF21, CPT-1a and ACOX1; (H–K) The mRNA expression of SIRT1, PPARα, CPT-1a and ACOX1. Data are presented as the mean ± SD (n = 6~8). ##p < 0.01 vs. NC group; *p < 0.05, **p < 0.01 vs. Model group.

Fig. 5. Effects ofL. plantarum Q16 on key proteins involved in hepatic lipid metabolism in HFD-fed obese mice. Data are presented as mean ± SD (n = 6). Different lowercase alphabet letters were significantly different at the level of P < 0.05.

Figure 3 Effect of methyl brevifolincarboxylate (MBC) on expression of lipogenesis and lipid oxidation mRNA and proteins in OA-treated SK-HEP-1 cells (A), and primary murine hepatocytes (B). Cells were treated with 0.5 mM of OA, and different concentrations of MBC (0, 20, 40, 60, and 80μM) for 48 h. Total RNA was isolated using a GENEzol reagent and mRNA was measured using qRT-PCR. Target gene mRNA levels were normalized to a reference gene β-actin. (C) Protein expression of FASN, ACC1, SREBP-1c, PPAR-α and (D) p-AMPK were detected by Western blot. All results are expressed as mean ± SD of three independent experiments. Data bars with similar letters were not significantly different (p ≤ 0.05).

FIGURE 5 EPC regulated the lipid metabolism-related genes and proteins inMAFLD rats. (A) mRNA abundances of FASN. (B) mRNA abundances of PPARα (PPARΑ). (C) mRNA abundances of PPARγ (PPARG). (D) mRNA abundances of RXRα. (E) mRNA abundances of CYP19A1. (F) mRNA abundances of NR3C1. (G) mRNA abundances of SREBP-1c. (H) mRNA abundances of HMGCR. (I) mRNA abundances of SCD. n = 6; (J) Relative expression of protein SCD. (K) Relative expression of protein PPARα. (L) Relative expression of protein FASN. (M) Relative expression of protein p-JNK. (N) Relative expression of protein p-NF-κB. (O) Relative expression of protein CYP19A1. (P) Relative expression of protein NR3C1. (Q-R) Representative immunoblotting images of β-actin, SCD, PPARα, FASN,CYP19A1, NR3C1, JNK, p-JNK, NF-κB, pNF-κB; n = 4, data are presented as mean ± SEM. One-way analysis of variance (ANOVA) was conducted for the group comparison. *p < 0.05, **p < 0.01, ***p < 0.001 vs MOD group. FASN, fatty acid synthase; PPARα/γ, peroxisome proliferator-activated receptor alpha/gamma; RXRa, retinoic acid receptor alpha; SREBP-1c, sterol regulatory element binding protein 1c; HMGCR, 3-hydroxy-3-methylglutaryl-coenzyme A reductase; SCD, Stearoyl-CoA desaturase; p-JNK, phosphorylation (p) -stress-activated protein kinase JNK; NF-κB, nuclear factor kappa B.

Fig. 8. Effect of β-PAE on AMPK signalling pathway. (A) The hepatic mRNA expressions of AMPK α , SREBP-1c and PPAR α . (B) Representative bands of p-AMPK α , AMPK α , SREBP-1c and PPAR α . (C) Quantitative results of Western blot bands densities of p-AMPK α / AMPK α , SREBP-1c and PPAR α . (D) Spearman correlation between hepatic CD36 expression and AMPK signalling pathway-related proteins indicators, respectively. Data are presented as the mean ± SD (n = 3 ~ 6). ## P < 0.01 vs. NC group; **P < 0.01 vs. Model group.