The enteric nervous system is affected by inflammatory bowel diseases (IBD). Gut microbiota ferments dietary fibers and produces short-chain fatty acids, such as Butyrate, which bind to G protein–coupled receptors, such as GPR41, and contribute to maintaining intestinal health. This work aimed to study the GPR41 in myenteric neurons and analyze the effect of Butyrate in mice submitted to experimental ulcerative colitis. The 2, 4, 6 trinitrobenzene sulfonic acid (TNBS) was injected intrarectally in C57BL/6 mice (Colitis). Sham group received ethanol (vehicle). One group was treated with 100 mg/kg of Sodium Butyrate (Butyrate), and the other groups received saline. Animals were euthanized 7 days after colitis induction. Analyzes demonstrated colocalization of GPR41 with neurons immunoreactive (-ir) to nNOS and ChAT-ir and absence of colocalization of the GPR41 with GFAP-ir glia. Quantitative results demonstrated losses of nNOS-ir, ChAT-ir, and GPR41-ir neurons in the Colitis group and Butyrate treatment attenuated neuronal loss. The number of GFAP-ir glia increased in the Colitis group, whereas Butyrate reduced the number of these cells. In addition, morphological alterations observed in the Colitis group were attenuated in the Butyrate group. The presence of GPR41 in myenteric neurons was identified, and the treatment with Butyrate attenuated the damage caused by experimental ulcerative colitis.

Background and Aims. Sepsis is defined as a life-threatening organ dysfunction due to a dysregulated host immune response to an infection. Curcumin is a yellow polyphenol derived from the rhizome of Curcuma longa with anti-inflammatory and antioxidant properties scientifically proven, a condition that allowed its use as a tool in the treatment of sepsis. Thus, the purpose of this article was to systematically review the evidence on the impact of curcumins anti-inflammatory effect on experimental sepsis. Methods. For this, the PubMed, MEDLINE, EMBASE, Scopus, Web of Science, and LILACS databases were used, and the research was not limited to a specific publication period. Only original articles in English using in vivo experimental models (rats or mice) of sepsis induction performed by administration of lipopolysaccharide (LPS) or cecal ligation and perforation surgery (CLP) were included in the study. Studies using curcumin in dry extract or with a high degree of purity were included. At initial screening, 546 articles were selected, and of these, 223 were eligible for primary evaluation. Finally, 12 articles with full text met all inclusion criteria. Our results showed that curcumin may inhibit sepsis-induced complications such as brain, heart, liver, lungs, and kidney damage. Curcumin can inhibit inflammatory factors, prevent oxidative stress, and regulate immune responses in sepsis. Additionally, curcumin increased significantly the survival rates after experimental sepsis in several studies. The modulation of the immune response and mortality by curcumin reinforces its protective effect on sepsis and indicates a potential therapeutic tool for the treatment of sepsis.

The enteric nervous system is affected by inflammatory bowel diseases (IBD). Gut microbiota ferment dietary fibers and produce short-chain fatty acids, such as Butyrate, which bind to G protein-coupled receptors, such as GPR41, and contribute to maintaining intestinal health. This work aimed to study the GPR41 in myenteric neurons and analyze the effect of Butyrate in mice submitted to experimental ulcerative colitis. The 2, 4, 6 trinitrobenzene sulfonic acid (TNBS) was injected intrarectally in C57BL/6 mice (Colitis). Sham group received ethanol (vehicle). One group was treated with 100mg/kg of Sodium Butyrate (Butyrate), and the other groups received saline. Animals were euthanized 7 days after colitis induction. Analyzes demonstrated colocalization of GPR41 with neurons immunoreactive (-ir) to nNOS and ChAT-ir, and absence of colocalization of the GPR41 with GFAP-ir glia. Quantitative results demonstrated losses of nNOS-ir, ChAT-ir, and GPR41-ir neurons in Colitis group, and Butyrate treatment attenuated neuronal loss. The number of GFAP-ir glia increased in Colitis group, whereas Butyrate reduced the number of these cells. In addition, morphological alterations observed in Colitis group were attenuated in Butyrate group. The presence of GPR41 in myenteric neurons was identified and the treatment with Butyrate attenuated the damage caused by experimental ulcerative colitis.

Background: Inflammatory bowel diseases, such as colitis, cause enteric nervous system dysfunction. Purinergic signaling through the P2X7 receptor (P2X7R) is activated during intestinal inflammation by extracellular ATP, but its role in chronic colitis remains unclear. Aim: Investigate the effects of an experimental colitis model on the ENS from mice knockout (KO) of P2X7R. Methods: Colitis was induced in wild‐type (WT) and KO mice by three cycles of Dextran Sodium Sulfate (DSS) (Cycles 1 and 2, 2% and Cycle 3, 1.5%) dissolved in drinking water for 5 days, followed by drinking water for the next 14 days (KO/DSS and WT/DSS groups). The KO/SHAM and WT/SHAM groups received water during the same period. The animals were euthanized after 57 days, and the distal colon was collected. Disease activity index and histological analysis were performed. Whole‐mount preparations of the myenteric plexus were analyzed by immunofluorescence for neuronal nitric oxide synthase (nNOS), acetylcholine transferase (ChAT), β3‐Tubulin, P2X7R, glial fibrillary acidic protein (GFAP), and S100β, and the inflammasome component NLRP3. Neuronal and glial densities were quantified. Key Results: Chronic DSS‐induced colitis decreased the nitrergic and cholinergic neurons, β3‐tubulin–ir neurons, and GFAP‐ir and S100β glial cells in WT/DSS and KO/DSS groups. P2X7R‐ir cells decreased in WT/DSS animals, and NLRP3‐ir cells increased mostly in WT/DSS, indicating inflammasome activation. There were changes in neuronal profile areas. These findings were significantly attenuated in P2X7R KO mice, indicating neuronal protection during chronic inflammation. Conclusions and Inferences: Experimental colitis affected the ENS of the distal colon. A slight neuronal attenuation of nNOS‐expressing neurons was observed in the P2X7RKO.