Protective effect of Gloeostereum incarnatum on ulcerative colitis via modulation of Nrf2/NF‑κB signaling in C57BL/6 mice

Gloeostereum incarnatum 通过调节 C57BL/6 小鼠中的 Nrf2/NF-κB 信号传导对溃疡性结肠炎产生保护作用

阅读:8
作者:Xiao Li, Xin Liu, Yongfeng Zhang, Yaqin Zhang, Shuyan Liu, Nan Zhang, Yu Li, Di Wang

Abstract

Chronic non‑specific inflammatory cell infiltration of the colon is generally considered to be the cause of ulcerative colitis (UC). Gloeostereum incarnatum (GI), a fungus rich in amino acids and fatty acids, exhibits a variety of biological functions. In the present study, GI was identified to contain 15 fatty acids, 17 amino acids and 11 metallic elements. The protective effect of GI against UC was investigated in C57BL/6 mice with UC induced by free drinking 3.5% dextran sulfate sodium (DSS). After a 21‑day oral administration, GI prevented weight loss, enhancement of the disease activity index and colonic pathological alterations in mice with UC. GI reduced the levels of pro‑inflammatory factors including interleukin (IL)‑1β, IL‑2, IL‑6 and IL‑12, tumor necrosis factor α and ‑β, interferon α and ‑γ, and pro‑oxidative factors including reactive oxygen species and nitric oxide. In addition, it enhanced the levels of immunological factors including immunoglobulin (Ig)A, IgM and IgG, and antioxidative factors including superoxide dismutase and catalase in the serum and/or colon tissues. GI enhanced the expression levels of nuclear factor erythroid 2‑related factor 2 (Nrf2) and its downstream proteins and suppressed the phosphorylation of NF‑κB signaling in colon tissues. Together, GI was shown to alleviate the physiological and pathological state of DSS‑induced UC in mice via its antioxidant and anti‑inflammatory functions, which may be associated with its modulation of the activation of Nrf2/NF‑κB signaling.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。