Fig. 2

Didymin protects AML12 cells against PA‐induced lipid deposition by activating Sirt1. A Principal component analysis (PCA) of the RNA-sequencing data of AML12 cells. B Volcano-plot of RNA-seq results for PA + Didymin vs. PA. C KEGG analysis of the enrichment pathways. D GO Process (GO-P) analysis. Heatmaps of gene expression profiles related to (E) mitochondrial function, (F) autophagy, and (G) apoptosis based on the RNA-seq data set. (n = 4) (H) Western blot analysis of Sirt1 in AML12 cells (n = 3). I Sirt1 deacetylase activity in AML12 cells (n = 3). J Interactive sites between Didymin and Sirt1 by docking analysis. K MST analysis of the interaction between Didymin and Sirt1 (n = 3). L Sirt1 recombinant protein deacetylase activity (n = 4). M TG contents in AML12 cells (n = 4). N Oil red O staining of AML12 cells (Scale bar = 20 μm). Data are expressed as mean ± SD. *P < 0.05, **P < 0.01, ****P < 0.0001 PA vs. PA + Didymin. ^#P < 0.05, ^##P < 0.01, ^###P < 0.001, ^####P < 0.0001 control vs. PA. PA palmitic acid, MST MicroScale Thermophoresis, TG triglyceride