College of Food Science, Shenyang Agricultural University, Shenyang, 110161, P. R. China.
Key Laboratory of Healthy Food Nutrition and Innovative Manufacturing of Liaoning, College of Food Science, Shenyang Agricultural University, Shenyang, 110161, P. R. China.
Mol Nutr Food Res. 2020 May;64(10):e1901315. doi: 10.1002/mnfr.201901315. Epub 2020 May 4.
This study investigates the modulatory effects of Lonicera caerulea L. polyphenols (LCPs) on the intestinal environment and lipopolysaccharide (LPS)-induced liver injury via the nuclear factor erythroid-2-related factor 2/heme oxygenase-1 (HO-1)/NQO1 and mitogen-activated protein kinase (MAPK) pathways in a rat model of oxidative stress damage (OSD).
To examine the prebiotic properties of LCP, a model of high-fat-diet-induced OSD is established using Sprague Dawley rats. In the colon, treatment with LCP for 8 weeks ameliorates enhanced intestinal permeability (glucagon-like peptide-2 content and occludin protein increase, whereas claudin-2 protein decreases), intestinal inflammation (levels of pro-inflammatory cytokines, such as tumor necrosis factor-α, interleukin-6, cyclooxygenase-2, and nuclear factor kappa-B p65 (NF-κB p65), decrease), and intestinal OSD (through regulation of the Nrf2/HO-1/NQO1 pathway). Moreover, LCP alleviates LPS-induced liver injury by suppressing the nuclear translocation of NF-κB p65 and activation of the MAPK signaling pathway. Additionally, Bacilli, Lactobacillales, Lactobacillaceae, Lactobacillus, Akkermansia, Actinobacteria, Proteobacteria, Rothia, and Blautia are found to be the key intestinal microbial taxa related to intestinal OSD and LPS-induced liver injury in rats.
LCP treatment potentially modulates the intestinal environment and alleviates liver injury by suppressing oxidative-stress-related pathways and altering the composition of the intestinal microbiota.
本研究通过核因子红细胞 2 相关因子 2/血红素加氧酶 1（HO-1）/NQO1 和丝裂原激活蛋白激酶（MAPK）通路，研究了蓝靛果多酚（LCPs）对氧化应激损伤（OSD）大鼠模型中肠道环境和脂多糖（LPS）诱导的肝损伤的调节作用。
为了研究 LCP 的益生元特性，我们使用 Sprague Dawley 大鼠建立了高脂肪饮食诱导的 OSD 模型。在结肠中，LCP 治疗 8 周可改善增强的肠道通透性（胰高血糖素样肽-2 含量和闭合蛋白增加，而闭合蛋白-2 蛋白减少）、肠道炎症（促炎细胞因子水平，如肿瘤坏死因子-α、白细胞介素-6、环氧化酶-2 和核因子 kappa-B p65（NF-κB p65）降低）和肠道 OSD（通过调节 Nrf2/HO-1/NQO1 通路）。此外，LCP 通过抑制 NF-κB p65 的核易位和激活 MAPK 信号通路来缓解 LPS 诱导的肝损伤。此外，发现芽孢杆菌、乳杆菌目、乳杆菌科、乳杆菌属、阿克曼氏菌属、放线菌、变形菌门、罗氏菌属和布劳特氏菌属是与大鼠肠道 OSD 和 LPS 诱导的肝损伤相关的关键肠道微生物类群。
LCP 治疗可能通过抑制氧化应激相关通路和改变肠道微生物群落组成来调节肠道环境并缓解肝损伤。
