丁酸盐保护了在实验性性结肠炎之后在小鼠中损失的肌肠神经元
Marcos A F Caetano1, Henrique I R Magalhães2, Jheniffer R L Duarte1
1Department of Anatomy, Institute of Biomedical Sciences, University of São Paulo, São Paulo 05508-000, Brazil.
Cells
|July 14, 2023
概括
丁酸盐是一种肠道微生物群的代谢物,可以保护肠道神经元免受实验性结肠炎的损伤. 这项研究在肌肠神经元中确定了GPR41,并表明丁酸盐治疗减弱了大肠炎引起的神经元损失和炎症.
科学领域:
- 神经胃肠病学 神经胃肠病学
- 炎症研究 炎症研究
- 微生物组-肠道-大脑轴
背景情况:
- 炎症性肠道疾病 (IBD) 影响肠道神经系统.
- 肠道微生物群产生短链脂肪酸,如丁酸盐,这些脂肪酸与G蛋白结合受体 (例如GPR41) 相互作用,以支持肠道健康.
研究的目的:
- 为了研究GPR41在肌肠神经元中的存在和作用.
- 在实验性性结肠炎的小鼠模型中评估Butyrate的治疗效果.
主要方法:
- 在C57BL/6小鼠中使用2,4,6三二硫酸 (TNBS) 诱导实验性性结肠炎.
- 用酸盐或盐水进行治疗.
- 肌肉神经元 (nNOS,ChAT) 和质神经元 (GFAP) 的免疫组合化学分析.
- 评估神经元和质细胞数量和形态变化.
主要成果:
- 发现GPR41与nNOS-ir和ChAT-ir神经神经元发生局部化,但与GFAP-ir神经并没有发生局部化.
- 大肠炎诱导了nNOS-ir,ChAT-ir和GPR41-ir神经元的显著损失,同时增加了GFAP-ir神经元.
- 丁酸盐治疗减轻了神经元损失,减少了质细胞活化,并在结肠炎模型中改善了形态变化.
结论:
- GPR41在参与调节肠道功能的肌肠神经元中表达.
- 丁酸盐的使用减轻了与实验性性结肠炎相关的神经元损伤和神经炎症,突出了其治疗潜力.
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