Jiangsu Collaborative Innovation Center of Chinese Medicinal, Resources Industrialization, Nanjing, Jiangsu 210023, P. R. China.
Jiangsu Key Laboratory for High Technology Research of TCM Formulae, Nanjing University of Chinese Medicine, Nanjing, Jiangsu 210023, P. R. China.
Am J Chin Med. 2023;51(6):1527-1546. doi: 10.1142/S0192415X23500696. Epub 2023 Jul 31.
Inflammatory bowel disease (IBD) is a recurrent disease associated with a potential risk of colorectal cancer. (AM), a Chinese herbal medicine, is known to alleviate IBD. However, its mechanism of action requires further clarification. Here, we focused on the role of IL-10 and the gut microbiota in the mechanism of action of AM. The effects of AM on intestinal inflammation, mucus production, and gut microbes were evaluated in dextran sodium sulfate (DSS)-induced acute and chronic IBD models and in IL-10-deficient mice (IL-10[Formula: see text]). AM exhibited protective effects on acute and chronic models of IBD in wild-type mice by restoring body weight and colon length, promoting IL-10 secretion, and decreasing TNF-[Formula: see text] levels. Moreover, AM alleviated inflammatory infiltration, increased mucin 2 transcription, and increased the number of goblet cells in the colon. On the contrary, these effects were diminished in IL-10[Formula: see text] mice, which implied that the effect of AM on intestinal inflammation is IL-10-dependent. A gut microbial sequencing analysis showed that gut microbial dysbiosis was modulated by AM intervention. The regulatory effects of AM on , , , , , and were dependent on IL-10. These results revealed that AM ameliorated IBD and modulated gut microbes by promoting IL-10 secretion, indicating that AM has the potential to improve IBD and that AM is IL-10-dependent.
炎症性肠病(IBD)是一种复发性疾病,存在结直肠癌的潜在风险。(AM)是一种中药,已知可缓解 IBD。然而,其作用机制仍需进一步阐明。在这里,我们专注于 AM 作用机制中的 IL-10 和肠道微生物群的作用。通过在葡聚糖硫酸钠(DSS)诱导的急性和慢性 IBD 模型以及 IL-10 缺陷型小鼠(IL-10[公式:见正文])中评估 AM 对肠道炎症、粘液产生和肠道微生物的影响。AM 通过恢复体重和结肠长度、促进 IL-10 分泌和降低 TNF-[公式:见正文]水平,对野生型小鼠的急性和慢性 IBD 模型表现出保护作用。此外,AM 减轻了炎症浸润,增加了粘蛋白 2 的转录,并增加了结肠中杯状细胞的数量。相反,这些作用在 IL-10[公式:见正文]小鼠中减弱,这表明 AM 对肠道炎症的作用依赖于 IL-10。肠道微生物测序分析表明,AM 干预调节了肠道微生物失调。AM 对 、 、 、 、 和 的调节作用依赖于 IL-10。这些结果表明,AM 通过促进 IL-10 分泌来改善 IBD 和调节肠道微生物群,表明 AM 具有改善 IBD 的潜力,并且 AM 依赖于 IL-10。