Exogenous Hydrogen Sulfide Inhibits Oral Mucosal Wound-induced Macrophage Activation via the NF-κB Pathway

Abstract

Objective

This study includes exploring (1) the production of endogenous hydrogen sulfide (H₂S) after mucosal wound generation and (2) the role of compensating the change in H₂S level post mucosal wound generation.

Methods and Materials

A mucosal wound model was established in female C57BL/6J mice. Wound tissues were collected to exam the change in the endogenous H₂S level. To examine the effect of decreased H₂S, GYY4137 was intraperitoneally injected into mice at 50 mg/kg/day 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.

Results

The production of endogenous H₂S and the expression of cystathionine b-synthase and cystathionine g-lyase in vivo was 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-κB signaling pathway.

Conclusion

The exogenous H₂S donor GYY4137 compensated for the reduced endogenous H₂S post mucosal wound generation and inhibited the induced M1 macrophage activation. Thus, appropriate H₂S supplementation may aid in controlling inflammation associated with mucosal wounds.

This article is protected by copyright. All rights reserved.

http://ift.tt/2npsNR2