Fig. 3
H2S inhibited IDO1 activity via H2S/NO crosstalk, and NO rather than H2S was an IDO1 inhibitor. a H2S donor upregulated the mRNA expression of iNOS in MCF-7 and SGC-7901 cells. Total RNA was extracted from the cells that were treated with different concentrations of NaHS for 24 h, and the mRNA expression levels of iNOS were analyzed by qPCR. b H2S deficiency downregulated the mRNA expression of Inos in Cse−/− mice. Total RNA was extracted from different tissues of the wt mice and Cse−/− mice, and the mRNA expression levels of Inos were analyzed by qPCR. c NO played an important role in the regulation of H2S on IDO1 activity. The cell supernatants were harvested, and kynurenine and tryptophan levels were measured by HPLC. d, e NO rather than H2S was a direct inhibitor of IDO1. Enzymatic assay of IDO1 was carried out with recombinant human IDO1 (rhIDO1) and different concentrations (0–400 μM) of H2S donors (NaHS, GYY4137), NO donor (SNP) and 1-L-MT. f Schematic diagram depicting the modulation of H2S on IDO1. All experiments repeated at least three times. Statistical significance was determined by Student’s t test (b) and one-way ANOVA followed by Dunnett’s test (a, c and d). *P < 0.05, **P < 0.01, n.s., no significant difference, bars show the group mean ± SEM