P45 Endogenous hydrogen sulfide suppresses intestinal inflammation through the regulation of macrophage polarization

详细信息    查看全文

• 作者：Yasuki Higashimura^a ; ^b ; Yuji Naito^a ; Tomohisa Takagi^a ; Ikuhiro Hirata^a ; Katsura Mizushima^a ; Toshikazu Yoshikawa^b
• 刊名：Nitric Oxide
• 出版年：30 May 2014
• 年：2014
• 卷：39
• 期：supp_S
• 页码：S29-S30
• 全文大小：52 K

文摘

Accumulating evidence shows the role of endogenous hydrogen sulfide (H₂S) in various disease, whereas its role of H₂S in intestinal inflammation. In addition, recent reports showed that H₂S modulates NF-kB signaling in macrophages, suggesting that H₂S could affect macrophage function. In this study, we studied the role of endogenous H₂S in a dextran sodium sulfate (DSS)-induced colitis model, particularly in relation to macrophage function.

Methods

Mice were treated with 8% DSS to induce colitis. DL-propargylglycine (PAG), an irreversible CSE (cystathionine gamma-lyase) inhibitor, and sodium sulfide (Na₂S), an H₂S donor, were administered intraperitoneally. The respective degrees of mucosal injury were evaluated macroscopically, histologically, and biochemistry. The effect of endogenous H₂S on macrophage function was evaluated using bone-marrow derived macrophages (BMDMs).

Results

CSE and CBS (cystathionine beta-synthase) expressions in the colonic mucosa were increased in DSS-treated mice. PAG enhanced DSS-induced colonic damage and myeloperoxidase activity. Meanwhile, Na₂S counteracted these effects of PAG. Furthermore, PAG-treated BMDMs manifested pro-inflammatory (M1), but not anti-inflammatory (M2) macrophages markers.

Conclusion

Our results demonstrated that endogenous H₂S inhibited the development of intestinal inflammation through the regulation of macrophage function. In conclusion, H₂S may be a novel therapeutic molecule in intestinal inflammation.