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Issue 69, 2016, Issue in Progress
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NaHS inhibits NF-κB signal against inflammation and oxidative stress in post-infectious irritable bowel syndrome

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Abstract

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 anti-inflammatory and antioxidant functions in TNF-α treated Caco-2 cells. Meanwhile, TNF-α exposure reduced cellular H2S level and cystathionine β-synthase (CBS), a H2S synthesis enzyme, further exacerbated TNF-α-induced inflammation in Caco-2 cells. NaHS reversed the effect of TNF-α and CBS siRNA on cellular H2S generation and inflammation. Furthermore, NaHS inhibited Trichinella spiralis induced NF-κB upregulation in Trichinella spiralis infected group. In conclusion, H2S plays a beneficial role in PI-IBS model and TNF-α induced inflammation in vitro, which may involve in NF-κB signaling pathway.

Graphical abstract: NaHS inhibits NF-κB signal against inflammation and oxidative stress in post-infectious irritable bowel syndrome

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Publication details

The article was received on 03 Jun 2016, accepted on 29 Jun 2016 and first published on 30 Jun 2016


Article type: Paper
DOI: 10.1039/C6RA13849G
Citation: RSC Adv., 2016,6, 64208-64214
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    NaHS inhibits NF-κB signal against inflammation and oxidative stress in post-infectious irritable bowel syndrome

    S. Yang, D. Deng, Y. Luo, Y. Wu, R. Zhu, K. Xue and Y. Zhou, RSC Adv., 2016, 6, 64208
    DOI: 10.1039/C6RA13849G

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