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Exogenous hydrogen sulfide inhibits oral mucosal wound‐induced macrophage activation via the NF ‐κB pathway
Author(s) -
Zhuang R,
Guo L,
Du J,
Wang S,
Li J,
Liu Y
Publication year - 2018
Publication title -
oral diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.953
H-Index - 87
eISSN - 1601-0825
pISSN - 1354-523X
DOI - 10.1111/odi.12838
Subject(s) - endogeny , inflammation , wound healing , in vivo , macrophage , medicine , chemistry , endocrinology , in vitro , biology , immunology , biochemistry , microbiology and biotechnology
Objective This study includes exploring (i) the production of endogenous hydrogen sulfide (H 2 S) after mucosal wound generation and (ii) the role of compensating the change in H 2 S level postmucosal wound generation. Methods and Materials A mucosal wound model was established in female C57BL/6J mice. Wound tissues were collected to examine the change in the endogenous H 2 S level. To examine the effect of decreased H 2 S, GYY 4137 was intraperitoneally injected into mice at 50 mg kg −1 day −1 before mucosal wounding to compensate for the decreased endogenous H 2 S. Finally, we confirmed the role of GYY 4137 in inhibiting the M1 phenotype macrophage activation induced by LPS in peritoneal macrophages and RAW 264.7. Results The production of endogenous H 2 S and the expression of cystathionine b‐synthase and cystathionine g‐lyase in vivo were reduced significantly in early stage after wound. GYY 4137 significantly inhibited the activation of the M1 phenotype induced by mucosal wound inflammation in vivo and LPS in vitro. Finally, we confirmed that GYY 4137 inhibited iNOS expression via the NF ‐κB signaling pathway. Conclusion The exogenous H 2 S donor GYY 4137 compensated for the reduced endogenous H 2 S postmucosal wound generation and inhibited the induced M1 macrophage activation. Thus, appropriate H 2 S supplementation may aid in controlling inflammation associated with mucosal wounds.