NaHS inhibits NF-kappa B signal against inflammation and oxidative stress in post-infectious irritable bowel syndrome

作者：Yang, Shenglan; Deng, Danfang; Luo, Yingying; Wu, Yanran; Zhu, Rui^*; Xue, Kaming; Zhou, Yanping

来源：RSC Advances, 2016, 6(69): 64208-64214.

DOI：10.1039/c6ra13849g

• HYDROGEN-SULFIDE PROTECTS
• MOUSE MODEL
• MICROBIOTA
• ALPHA
• MICE
• MODULATION
• ACTIVATION
• PATHWAYS
• FIBROSIS
• CYSTEINE

In this study, the alleviating role of hydrogen sulfide (H2S) was investigated in a Post-Infectious Irritable Bowel Syndrome (PI-IBS) murine model and Caco-2 cells. Murine PI-IBS model was established using Trichinella spiralis infection and the results showed that mice infected with Trichinella spiralis exhibited marked intestinal inflammatory response and oxidative injury. NaHS, a H2S donor, injection markedly alleviated inflammatory response and oxidative injury and in vitro data further confirmed the antiinflammatory and antioxidant functions in TNF-alpha treated Caco-2 cells. Meanwhile, TNF-alpha exposure reduced cellular H2S level and cystathionine beta-synthase (CBS), a H2S synthesis enzyme, further exacerbated TNF-alpha-induced inflammation in Caco-2 cells. NaHS reversed the effect of TNF-alpha and CBS siRNA on cellular H2S generation and inflammation. Furthermore, NaHS inhibited Trichinella spiralis induced NF-kappa B upregulation in Trichinella spiralis infected group. In conclusion, H2S plays a beneficial role in PI-IBS model and TNF-alpha induced inflammation in vitro, which may involve in NF-kappa B signaling pathway.

• 出版日期2016
• 单位华中科技大学