College of Life Science and Engineering, Northwest Minzu University, Lanzhou, 730100, China.
Key Laboratory of Biotechnology and Bioengineering of State Ethnic Affairs Commission, Biomedical Research Center, Northwest Minzu University, Lanzhou, 730030, China.
Eur J Nutr. 2024 Nov 28;64(1):32. doi: 10.1007/s00394-024-03520-w.
In order to address the global public health concern of colitis, this study was conducted to investigate the beneficial effect of Lactobacillus plantarum LR002 (LR) on the remission of ulcerative colitis (UC) in mice and to explore the possible underlying mechanisms.
The effect of LR on UC was analyzed by using dextran sodium sulfate (DSS)-induced UC model in mice (n = 9). To assess the therapeutic effect of LR on UC in mice, the disease activity index (DAI) of mice, histopathological alterations, intestinal epithelial barrier integrity, and intestinal microflora were determined.
The results demonstrated a reduction in the DSS-induced DAI in UC mice. Additionally, it mitigated colon shortening, minimized intestinal tissue damage, and preserved intestinal tight junction proteins (Claudin-3, Occludin, and ZO-1). LR reduced the levels of proinflammatory cytokines (IL-1β, IL-6, and TNF-α) and oxidative mediators (MPO, SOD and MDA) in the colon of UC mice, which could also alleviate the imbalance of intestinal flora in UC mice, increase the abundance of Prevotellaceae, and Ligilactobacillus, and decrease the abundance of Bacteroidaceae and Eubacteriumrum. LR can also increase the levels of PPARγ in the nucleus and inhibit the MAPK/NF-ĸB signaling pathway in UC mice. Besides, the reduction of the content of short-chain fatty acid (SCFAs) in the colon of UC mice was relieved.
The above results forge a scientific basis for LR as natural anti-inflammatory food to improve the imbalance of inflammatory intestinal flora and promote intestinal health.
为了解决结肠炎这一全球公共卫生关注问题，本研究旨在探讨植物乳杆菌 LR002（LR）对溃疡性结肠炎（UC）缓解的有益作用，并探讨其可能的潜在机制。
采用葡聚糖硫酸钠（DSS）诱导的 UC 模型小鼠（n=9）分析 LR 对 UC 的影响。为评估 LR 对 UC 小鼠的治疗作用，测定了小鼠疾病活动指数（DAI）、组织病理学改变、肠上皮屏障完整性和肠道微生物群。
结果表明，LR 可降低 DSS 诱导的 UC 小鼠 DAI。此外，LR 还减轻了结肠缩短，最小化了肠道组织损伤，并保护了肠道紧密连接蛋白（Claudin-3、Occludin 和 ZO-1）。LR 降低了 UC 小鼠结肠中促炎细胞因子（IL-1β、IL-6 和 TNF-α）和氧化介质（MPO、SOD 和 MDA）的水平，还可以减轻 UC 小鼠肠道菌群失衡，增加普雷沃氏菌科和 ligilactobacillus 的丰度，降低拟杆菌科和真杆菌属的丰度。LR 还可以增加 UC 小鼠细胞核中 PPARγ 的水平，并抑制 MAPK/NF-ĸB 信号通路。此外，UC 小鼠结肠中短链脂肪酸（SCFAs）含量的减少也得到了缓解。
上述结果为 LR 作为天然抗炎食品改善炎症性肠道菌群失衡和促进肠道健康提供了科学依据。
