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

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.