title: Hydrogen sulfide attenuates the inflammatory response in a mouse burn injury model.
abstract: Hydrogen sulfide (H2S) is a naturally occurring gaseous transmitter, which is important in normal physiology and disease. In the present study, the involvement of H2S in the regulation of the immune response induced by burn injury was investigated in mice. Adult male C57BL/6 mice were subjected to burn injuries and treated with vehicle (0.9% sodium chloride, NaCl; 100 ml/kg body weight; subcutaneously, s.c.) or the H2S donor (sodium hydrosulfide, NaHS; 2 mg/kg body weight; s.c.). Compared with the controls, mice which received burn injuries exhibited a significant decrease in plasma H2S levels. Moreover, the levels of tumor necrosis factor (TNF)‑α, interleukin (IL)‑6 and IL‑8 significantly increased, while IL‑10 levels were decreased, compared with that of the controls in the plasma of mice subjected to burn injuries. Myeloperoxidase (MPO) activity in the liver tissue of injured mice was also markedly higher compared with that of the control group. However, the administration of NaHS significantly decreased the levels of TNF‑α, IL‑6 and IL‑8 but increased the levels of IL‑10 in the plasma of mice subjected to burn injuries. In addition, the MPO activity was decreased by NaHS. These results suggested that H2S regulates the inflammatory response induced by burn injury by modulating the levels of TNF‑α, IL‑6, IL‑8 and IL‑10. Thus, it was proposed that the administration of the H2S donor, NaHS, may be a useful therapy against the exaggerated immune response that is associated with burn injury.
authors.affiliation: College of Pharmacy, Guilin Medical University, Guilin, Guangxi 541004, P.R. China.
authors.forename: Jianhong
authors.initials: J
authors.lastname: Zeng
authors.forename: Xianhe
authors.initials: X
authors.lastname: Lin
authors.forename: Haipeng
authors.initials: H
authors.lastname: Fan
authors.forename: Changqing
authors.initials: C
authors.lastname: Li
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D002056:Burns / Q000097:blood / Q000188:drug therapy* / Q000276:immunology; D006862:Hydrogen Sulfide / Q000097:blood; D018836:Inflammation Mediators / Q000097:blood; D016753:Interleukin-10 / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D016209:Interleukin-8 / Q000097:blood; D008099:Liver / Q000201:enzymology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009195:Peroxidase / Q000378:metabolism; D013440:Sulfides / Q000494:pharmacology*; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D000893:Anti-Inflammatory Agents; C556062:IL10 protein, mouse; D018836:Inflammation Mediators; D015850:Interleukin-6; D016209:Interleukin-8; D013440:Sulfides; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D009195:Peroxidase; C025451:sodium bisulfide; D006862:Hydrogen Sulfide