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The protective role of phloretin against dextran sulfate sodium-induced ulcerative colitis in mice
Food & Function ( IF 6.1 ) Pub Date : 2018-12-21 00:00:00 , DOI: 10.1039/c8fo01699b
Zecai Zhang 1, 2, 3, 4, 5 , Shan Li 1, 2, 3, 4 , Hongyang Cao 1, 2, 3, 4 , Peng Shen 1, 2, 3, 4 , Jiuxi Liu 1, 2, 3, 4 , Yunhe Fu 1, 2, 3, 4 , Yongguo Cao 1, 2, 3, 4 , Naisheng Zhang 1, 2, 3, 4
Affiliation  

Phloretin, a dihydrogen chalcone flavonoid, is mainly isolated from apples and strawberries. Phloretin has been proven to have many biological activities such as anti-inflammatory and anti-oxidative. Herein, we investigated the protective efficacy and potential mechanism of phloretin in dextran sulfate sodium (DSS)-induced ulcerative colitis (UC) in mice. The results showed that phloretin resulted in a reduced DSS-induced disease activity index (DAI), colon length shortening and colonic pathological damage. The levels of pro-inflammatory cytokines in the colon were also decreased by the administration of phloretin. Exploration of the potential mechanism demonstrated that phloretin suppressed the inflammatory response by regulating the nuclear factor-κB (NF-κB), toll-like receptor 4 (TLR4) and peroxisome proliferator-activated receptor γ (PPARγ) pathways. Phloretin also inhibited the DSS-induced (NOD)-like receptor family and pyrin domain containing 3 (NLRP3) inflammasome activations. Further studies found that phloretin reduced key markers of oxidative stress as well as regulated the expression of zonula occludens-1 (ZO-1) and occludin. Interestingly, the concentration of serum lipopolysaccharide (LPS) was significantly decreased. Escherichia coli (E. coli) and Lactobacillus levels were also re-balanced after phloretin treatment. These results indicate that phloretin might be a new dietary strategy for the treatment of UC.

中文翻译:

伞菌素对硫酸葡聚糖钠诱导的小鼠溃疡性结肠炎的保护作用

蝶呤是一种二氢查尔酮类黄酮,主要从苹果和草莓中分离出来。磷脂已被证明具有许多生物活性,例如抗炎和抗氧化。在这里,我们调查了佛瑞丁在硫酸右旋糖酐钠(DSS)诱导的小鼠溃疡性结肠炎(UC)中的保护作用和潜在机制。结果表明,促肾上腺皮质激素导致DSS诱导的疾病活动指数(DAI)降低,结肠长度缩短和结肠病理损害。施用促胰泌素后,结肠中促炎性细胞因子的水平也降低了。探索潜在的机制表明,伞菌素通过调节核因子-κB(NF-κB)抑制炎症反应,Toll样受体4(TLR4)和过氧化物酶体增殖物激活的受体γ(PPARγ)途径。荧光素还抑制DSS诱导的(NOD)样受体家族和含有3(NLRP3)炎性小体活化的吡喃结构域。进一步的研究发现,phloretin减少了氧化应激的关键标志物,并调节了小带闭合蛋白1(ZO-1)和闭合蛋白的表达。有趣的是,血清脂多糖(LPS)的浓度明显降低。毛菌素治疗后大肠杆菌E. coli)和乳酸杆菌水平也重新达到平衡。这些结果表明,促肾上腺皮质激素可能是治疗UC的新饮食策略。
更新日期:2018-12-21
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