Allyl isothiocyanate ameliorates metabolic dysfunction-associated steatotic liver disease via vitamin D receptors in hepatocytes

Figure 1 Palmitate acid induces lipid accumulation by promoting hepatic lipogenesis and inhibiting fatty acid β-oxidation in hepatocytes. AML-12 cells were treated with 300 μM palmitate acid (PA) for 24 hours to establish an in vitro model of metabolic dysfunction-associated steatotic liver disease. A: Intracellular triglyceride content in PA-stimulated AML-12 cells (n = 3/group); B: The protein expressions of lipogenesis target genes, fatty acid synthase, and acetyl-CoA carboxylase 1, were detected via Western blotting; C: The protein expressions of genes involved in fatty acid β-oxidation, such as peroxisome proliferator-activated receptor α and peroxisome proliferator-activated receptor gamma coactivator 1α, were detected via Western blotting. Data are presented as the mean ± SD. ^cP < 0.001. P value calculated between groups. TG: Triglyceride; PA: Palmitate acid; FA: Fatty acid; FAS: Fatty acid synthase; GAPDH: Glyceraldehyde-3-phosphate dehydrogenase; ACC1: Acetyl-CoA carboxylase 1; PPAR: Peroxisome proliferator-activated receptor; PGC-1α: Peroxisome proliferator-activated receptor gamma coactivator 1α.