Fig. 6

NO inhibited the adipogenic capacity of PDLSCs through the JNK/MAPK pathway. a,b Oil Red O staining indicating that sodium nitroprusside (SNP) treatment downregulated the level of adipogenesis, while blocking the JNK/MAPK signaling pathway reversed this effect. Data are representative of three independent experiments. **P < 0.01. c Real-time RT-PCR showing that l-NMMA treatment induced the expression of lipoprotein lipase (LPL), peroxisome proliferator-activated receptor (PPAR)γ, and CCAAT-enhancer binding protein (C/EBP)α mRNA, but activating the JNK/MAPK pathway largely reversed their upregulation. All experiments are representative of three replicates. **P < 0.01. d Western blot showing that SNP treatment repressed the expression of PPARγ and phosphorylated c-Jun N-terminal kinase (p-JNK), while JNK inhibitor treatment enhanced the expression of these markers