Exogenous hydrogen sulfide inhibits oral mucosal wound-induced macrophage activation via the NF-B pathway

ObjectiveThis study includes exploring (i) the production of endogenous hydrogen sulfide (H2S) after mucosal wound generation and (ii) the role of compensating the change in H2S level postmucosal wound generation. Methods and MaterialsA mucosal wound model was established in female C57BL/6J mice. Wound tissues were collected to examine the change in the endogenous H2S level. To examine the effect of decreased H2S, GYY4137 was intraperitoneally injected into mice at 50mgkg(-1)day(-1) before mucosal wounding to compensate for the decreased endogenous H2S. Finally, we confirmed the role of GYY4137 in inhibiting the M1 phenotype macrophage activation induced by LPS in peritoneal macrophages and RAW264.7. ResultsThe production of endogenous H2S and the expression of cystathionine b-synthase and cystathionine g-lyase in vivo were reduced significantly in early stage after wound. GYY4137 significantly inhibited the activation of the M1 phenotype induced by mucosal wound inflammation in vivo and LPS in vitro. Finally, we confirmed that GYY4137 inhibited iNOS expression via the NF-B signaling pathway. ConclusionThe exogenous H2S donor GYY4137 compensated for the reduced endogenous H2S postmucosal wound generation and inhibited the induced M1 macrophage activation. Thus, appropriate H2S supplementation may aid in controlling inflammation associated with mucosal wounds.