Fig. 4
NO promoted the osteogenic capacity of PDLSCs through the JNK/MAPK pathway. a,b Western blot showing that phosphorylated c-Jun N-terminal kinase (p-JNK) was decreased when NO generation was blocked by l-NG-monomethyl arginine (l-NMMA) during osteogenic or adipogenic induction, while sodium nitroprusside (SNP) significantly increased the expression of p-JNK. c Alkaline phosphatase (ALP) staining showing that SNP treatment upregulated the level of ALP, while blocking the JNK/MAPK signaling pathway restrained this SNP-induced ALP expression. **P < 0.01. d Alizarin Red staining showed that SNP treatment significantly increased the formation of mineralized nodules in PDLSCs, and this effect was reversed by inhibiting JNK/MAPK. Data are representative of three independent experiments. **P < 0.01. e Calcium concentration measurement showing that blocking the JNK/MAPK signaling pathway reduces SNP-induced calcium levels. **P < 0.01. f Real-time RT-PCR analysis of osteogenic marker expression during differentiation. Runt-related transcription factor 2 (Runx2), osterix (OSX), and osteopontin (OPN) mRNA levels were significantly increased by SNP, while JNK inhibitor partially eliminated the influence of SNP. All experiments are representative of three replicates. **P < 0.01. g Western blot showing that SNP treatment upregulated ALP, Runx2, and p-JNK, and JNK inhibitor treatment significantly reduced this upregulation