Department of Anatomy, Institute of Biomedical Sciences, University of São Paulo, São Paulo 05508-000, Brazil.
Department of Surgery, School of Veterinary Medicine and Animal Sciences, University of São Paulo, São Paulo 05508-270, Brazil.
Cells. 2023 Jun 21;12(13):1672. doi: 10.3390/cells12131672.
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.
肠神经系统受炎症性肠病（IBD）的影响。肠道微生物群发酵膳食纤维并产生短链脂肪酸，如丁酸盐，其与 G 蛋白偶联受体（如 GPR41）结合，有助于维持肠道健康。本工作旨在研究肌间神经元中的 GPR41，并分析丁酸盐对实验性溃疡性结肠炎小鼠的影响。2,4,6-三硝基苯磺酸（TNBS）被直肠内注射到 C57BL/6 小鼠（结肠炎）中。假手术组接受乙醇（载体）。一组用 100mg/kg 的丁酸钠（丁酸盐）治疗，其他组用生理盐水处理。在结肠炎诱导后 7 天处死动物。分析显示 GPR41 与神经元免疫反应性（-ir）到 nNOS 和 ChAT-ir 共定位，而 GPR41 与 GFAP-ir 胶质细胞无共定位。定量结果显示 nNOS-ir、ChAT-ir 和 GPR41-ir 神经元在结肠炎组中的损失，而丁酸盐治疗减轻了神经元的损失。GFAP-ir 胶质细胞的数量在结肠炎组中增加，而丁酸盐减少了这些细胞的数量。此外，在丁酸盐组中减轻了结肠炎组中观察到的形态改变。鉴定出肌间神经元中的 GPR41，并用丁酸盐处理减轻了实验性溃疡性结肠炎引起的损伤。
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