GPA peptide enhances Nur77 expression in intestinal epithelial cells to exert a protective effect against DSS‐induced colitis

Abstract

Ulcerative colitis (UC), an intractable inflammatory bowel disease (IBD), is a chronic and idiopathic inflammatory disease which affects the colon, resulting in weight loss, diarrhea, rectal bleeding, and abdominal pain. 1-4 In the inflamed tissue of patients with UC, the tight junctions of epithelium are disrupted, enabling microbes to migrate from the lumen into the lamina propria. Once the NF-κB pathway is activated, large amounts of pro-inflammatory cytokines will be produced to cause a cycle of uncontrolled inflammation, which results in severe damage to the intestinal wall. 5 Hence,

Konjac oligosaccharides attenuate DSS-induced ulcerative colitis in mice: mechanistic insights

“…After histological examination, the histopathology grading scores for colonic sections were measured as previously described with slight modifications. 21…”

GPA Peptide Attenuates Sepsis‐Induced Acute Lung Injury in Mice via Inhibiting Oxidative Stress and Pyroptosis of Alveolar Macrophage

“…GPA peptide was procured from Top Peptide Biotechnology Co., Ltd. (Shanghai, China). The dosage of GPA peptide was chosen based on prior studies [ 9 , 13 ]. Administration of GPA peptide (50, 100, or 150 mg/kg) to the GPA peptide cohort and CLP+GPA peptide cohort was done via oral gavage at one dose each day for 7 days prior to and during CLP treatment.…”

“…Gly-Pro-Ala (GPA) peptide, extracted from gelatin hydrolysate of fish skin, has been proven to have antioxidant and anti-inflammatory effects either in vivo or in vitro [ 8 ]. Recent literature demonstrated that Nur77 mitochondrial translocation is induced by GPA peptide, which impedes inflammation and oxidative stress by promoting autophagy subsequently [ 9 ]. Moreover, GPA peptide was also discovered as a potential therapy in DSS-induced colitis through blocking ROS and mtDNA production along with inhibiting pyroptosis in macrophages and the activation of NLRP3 inflammasome [ 10 ].…”

NR4A1 suppresses pyroptosis by transcriptionally inhibiting NLRP3 and IL‐1β and co‐localizing with NLRP3 in trans‐Golgi to alleviate pathogenic bacteria‐induced colitis

“…Inflammatory bowel disease (IBD) is a chronic and intractable digestive tract inflammatory disease that affects the millions of people; blocking immune responses and inflammatory cytokines have become effective strategies for treating colitis. NR4A1 (also known as TR3, NGFIB or Nur77), a member of the nuclear receptor NR4A family, exerts a protective role in colitis, 1 , 2 however, its effect and mechanism on pyroptosis or NLRP3 inflammasome is still unclear.…”