Li Liwen, Long Qi, Deng Na, Tan Zhoujin
School of Traditional Chinese Medicine, Hunan University of Chinese Medicine, Changsha, China.
Laboratory of Chinese Medicine Prescription and Syndromes Translational Medicine, Changsha, China.
Front Microbiol. 2025 Apr 29;16:1567971. doi: 10.3389/fmicb.2025.1567971. eCollection 2025.
To establish and evaluate an IBS-D mouse model with Spleen-Kidney Yang Deficiency, explore the microecological mechanisms of IBS-D, and provide experimental evidence for the clinical diagnosis and treatment of IBS-D with Spleen-Kidney Yang Deficiency.
SPF-grade female Kunming mice were used to establish an IBS-D model with Spleen-Kidney Yang Deficiency through adenine administration combined with restraint-clamping tail. (1) Clinical symptoms and signs were assessed using diagnostic criteria. (2) The small intestine structure was examined via Alcian blue staining, and intestinal barrier markers like D-LA (D-lactate) and DAO (diamine oxidase) were measured by ELISA to assess pathophysiological changes. (3) 16S rRNA gene sequencing was performed to analyze the intestinal microbiota.
(I) The model mice exhibited symptoms of IBS-D with Spleen-Kidney Yang Deficiency. (II) ELISA and alcian blue staining revealed elevated levels of D-LA and DAO activity in the model group, indicating damage to the intestinal mucosal barrier structure. (III) Analysis of the intestinal mucosal microbiota in the model group revealed differences in dominant and characteristic bacteria at various taxonomic levels compared with those in the normal group, reflecting an imbalance in the intestinal mucosal microbiota. (IV) and are associated with mucosal barrier damage in mice modeled by adenine administration combined with restraint-clamping tail.
The combination of adenine administration with restraint-clamping tail can be used to successfully establish an IBS-D mouse model with Spleen-Kidney Yang Deficiency. This model leads to damage to the intestinal mucosal structure. , , , , and may serve as potential biological markers for the intestinal mucosal microbiota.
建立并评价脾肾阳虚型腹泻型肠易激综合征（IBS-D）小鼠模型，探讨IBS-D的微生态机制，为脾肾阳虚型IBS-D的临床诊疗提供实验依据。
采用SPF级雌性昆明小鼠，通过腺嘌呤灌胃联合夹尾束缚建立脾肾阳虚型IBS-D模型。（1）运用诊断标准评估临床症状和体征。（2）通过阿尔辛蓝染色检查小肠结构，采用酶联免疫吸附测定法（ELISA）检测肠屏障标志物如D-乳酸（D-LA）和二胺氧化酶（DAO），以评估病理生理变化。（3）进行16S rRNA基因测序分析肠道微生物群。
（I）模型小鼠表现出脾肾阳虚型IBS-D的症状。（II）ELISA和阿尔辛蓝染色显示模型组D-LA水平升高和DAO活性增强，表明肠黏膜屏障结构受损。（III）模型组肠黏膜微生物群分析显示，与正常组相比，各分类水平上的优势菌和特征菌存在差异，反映出肠黏膜微生物群失衡。（IV）[此处原文缺失相关内容]与腺嘌呤灌胃联合夹尾束缚建模小鼠的黏膜屏障损伤有关。
腺嘌呤灌胃联合夹尾束缚可成功建立脾肾阳虚型IBS-D小鼠模型。该模型导致肠黏膜结构受损。[此处原文缺失相关内容]、[此处原文缺失相关内容]、[此处原文缺失相关内容]、[此处原文缺失相关内容]和[此处原文缺失相关内容]可能作为肠黏膜微生物群的潜在生物标志物。
