Allyl isothiocyanate ameliorates lipid accumulation and inflammation in nonalcoholic fatty liver disease via the Sirt1/AMPK and NF-κB signaling pathways

Figure 4 Allyl isothiocyanate alleviates palmitate acid-induced lipid accumulation in vitro. Palmitate acid (200 μmo/L)-stimulated AML-12 cells were treated with allyl isothiocyanate (20 μmo/L) or dimethyl sulfoxide (vehicle) for 24 h. A: Cytotoxicity was measured by the lactate dehydrogenase (LDH) release method in AML-12 cells (n = 3/group). B: Cell viability was measured using the cholecystokinin-8 (CCK-8) assay in AML-12 cells (n = 3/group). C: Intracellular triglyceride (TG) content in AML-12 cells (n = 3/group). And D: Representative image of oil red O staining of AML-12 cells in different groups. Scale bar in panel represents 100 μm. Data are presented as the mean ± SD. ^bP < 0.01 vs 0 μmol/L AITC, ^dP < 0.01 vs PA(-) AITC(-), ^fP < 0.01 vs PA(+) AITC(-). LDH: Lactate dehydrogenase; CCK-8: Cholecystokinin-8; TG: Triglyceride; NC: Negative control; PA: Palmitate acid: AITC: Allyl isothiocyanate.