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

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.

Sinapic Acid Ameliorates Acetic Acid-Induced Ulcerative Colitis in Rats by Suppressing Inflammation, Oxidative Stress, and Apoptosis

“…In the present investigation, AA induced a significant escalation in levels of NF-κB, TNF-α, IL-6, and oxidative stress and depletion of GSH and CAT in AA-induced colon tissues. These findings further corroborate and reinforce studies that claim that AA aggravates up-regulation of NF-κB and inflammatory cytokines levels in an experimental colitis model in rats [8,23,37]. In contrast, SA 40 mg/kg pretreatment significantly and abridged these elevated levels [18,37,50].…”

“…In rodent models, oral or systemic administration of phenolic acids such as epigallocatechin gallate, resveratrol, quercetin, and curcumin downregulate nuclear factor (NF-κ B)-dependent gene expression and upregulate phase II detoxifying and antioxidant proteins. Polyphenols prevented UC [20][21][22][23]. Yet no studies have been performed to assess the protective effect of SA against AA-induced UC in a rat model and mechanisms remain vague.…”

Anti-Inflammatory Effects of Rosmarinic Acid-Loaded Nanovesicles in Acute Colitis through Modulation of NLRP3 Inflammasome

“…Upon oxidative stress, Nrf2 induces nuclear transcription of endogenous antioxidant enzymes, such as HO-1 [5]. Activation of the Nrf2/HO-1 pathway has been reported to attenuate the inflammatory response in experimental colitis [6], while suppressing Nrf2 increased inflammation and oxidative stress [7]. Thus, pharmacological induction of this pathway may be a useful strategy for IBD treatment.…”

Effects of Medicinal Plants and Phytochemicals in Nrf2 Pathways during Inflammatory Bowel Diseases and Related Colorectal Cancer: A Comprehensive Review

“…Li et al [ 183 ] explored Gloeostereum incarnatum , a fungus rich in amino and fatty acids, on UC via modulation of Nrf2/NF-κB signaling in C57BL/6 mice. The use of the fungus reduced ROS and pro-inflammatory cytokines, such as IL-1β, IL-2, IL-6, IL-12, TNF-α, TNF-β, IFN-α, and IFN-γ.…”