State Key Laboratory of Food Science and Resources, No. 235 Nanjing East Road, Nanchang, Jiangxi 330047, PR China.
Institute of Biological Resources, Jiangxi Academy of Sciences, Nanchang 330096, China.
Int J Biol Macromol. 2024 Oct;278(Pt 1):134203. doi: 10.1016/j.ijbiomac.2024.134203. Epub 2024 Aug 6.
This study aimed to investigate the potential alleviating effect of Epimedium polysaccharide (EP) on intestinal inflammation aggravated by Porphyromonas gingivalis (Pg). P. gingivalis, an oral pathogen, may play a role in intestinal inflammation, highlighting the necessity to explore substances capable of inhibiting its pathogenicity. Initially, in vitro screening experiments utilizing co-culturing and quantitative polymerase chain reaction revealed that EP significantly inhibited the growth of P. gingivalis and the levels of virulence genes, including Kgp and RgpA. Subsequent mouse experiments demonstrated that EP notably ameliorated Pg-aggravated weight loss, disease activity index, histopathological lesions, and disruption of intestinal barrier integrity, evidenced by a reduction in tight junction protein levels. Flow cytometry analysis further illustrated that EP attenuated Pg-induced Th17 differentiation and Th17-related cytokines, such as IL-17 and IL-6. Additionally, 16S rRNA amplicon sequencing analysis elucidated that EP significantly mitigated Pg-induced gut microbiota dysbiosis, enriching potentially beneficial microbes, including Akkermansia and Bifidobacterium. The metabolomic analysis provided further insight, indicating that EP intervention altered the accumulation of relevant intestinal metabolites and exhibited correlations with disease indicators. In conclusion, our research suggested that EP holds promise as a prospective therapeutic agent for alleviating P. gingivalis-aggravated intestinal inflammation.
本研究旨在探讨淫羊藿多糖(EP)对牙龈卟啉单胞菌(Pg)加重的肠道炎症的潜在缓解作用。口腔病原体Pg 可能在肠道炎症中发挥作用,这凸显了探索能够抑制其致病性的物质的必要性。首先,通过共培养和实时定量聚合酶链反应的体外筛选实验表明,EP 显著抑制了 P. gingivalis 的生长和毒力基因(包括 Kgp 和 RgpA)的水平。随后的小鼠实验表明,EP 显著改善了 Pg 加重的体重减轻、疾病活动指数、组织病理学损伤和肠道屏障完整性的破坏,这表现为紧密连接蛋白水平的降低。流式细胞术分析进一步表明,EP 减弱了 Pg 诱导的 Th17 分化和 Th17 相关细胞因子,如 IL-17 和 IL-6。此外,16S rRNA 扩增子测序分析表明,EP 显著减轻了 Pg 诱导的肠道微生物群落失调,丰富了潜在有益的微生物,包括 Akkermansia 和双歧杆菌。代谢组学分析提供了进一步的见解,表明 EP 干预改变了相关肠道代谢物的积累,并与疾病指标相关。总之,我们的研究表明,EP 有望成为缓解 P. gingivalis 加重的肠道炎症的一种有前途的治疗剂。