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图尔奇。蜂蜜通过/途径预防DSS诱导的人Caco-2细胞中的炎症反应并抑制铁死亡。 (注:原文中“by / Pathway”表述不完整准确,可能会影响理解的精准度)

Turcz. Honey Prevents Inflammation Response and Inhibits Ferroptosis by / Pathway in DSS-Induced Human Caco-2 Cells.

作者信息

Ren Caijun, Zhu Yuying, Li Qiangqiang, Wang Miao, Qi Suzhen, Sun Dandan, Wu Liming, Zhao Liuwei

机构信息

State Key Laboratory of Resource Insects, Institute of Apicultural Research, Chinese Academy of Agricultural Sciences, Beijing 100093, China.

Risk Assessment Laboratory for Bee Products Quality and Safety of Ministry of Agriculture, Beijing 100093, China.

出版信息

Antioxidants (Basel). 2024 Jul 25;13(8):900. doi: 10.3390/antiox13080900.

Abstract

Turcz. () honey, a monofloral honey, has garnered increased attention due to its origin in the plant. A previous study has shown that honey can ameliorate inflammation. In this study, we aimed to investigate the effects of honey extract and its biomarker (Trifolin) on DSS-induced ulcerative colitis (UC). Our results demonstrated that honey extract and Trifolin significantly increased the expression levels of the tight junction cytokines and . Additionally, they decreased the pro-inflammatory factors and and enhanced the antioxidant factors and . Based on metabolomic analyses, honey extract and Trifolin regulated the progression of UC by inhibiting ferroptosis. Mechanistically, they improved the levels of SOD and iron load, increased the GSH/GSSG ratio, reduced MDA content and ROS release, and upregulated the / pathway, thereby inhibiting DSS-induced UC. Moreover, the expression levels of ferroptosis-related genes indicated that they decreased , , and while increasing expression to resist ferroptosis. In conclusion, our study found that honey improves DSS-induced UC by inhibiting ferroptosis by activating the / pathway. These findings further elucidate the understanding of anti-inflammatory and antioxidant activities of honey.

摘要

图尔采蜂蜜(Turcz. () honey),一种单花蜜,因其源自[具体植物名称]植物而受到越来越多的关注。先前的一项研究表明,[该植物名称]蜂蜜可以改善炎症。在本研究中,我们旨在研究[该植物名称]蜂蜜提取物及其生物标志物(三叶豆苷)对葡聚糖硫酸钠(DSS)诱导的溃疡性结肠炎(UC)的影响。我们的结果表明,[该植物名称]蜂蜜提取物和三叶豆苷显著提高了紧密连接细胞因子[具体细胞因子名称1]和[具体细胞因子名称2]的表达水平。此外,它们降低了促炎因子[具体促炎因子名称1]和[具体促炎因子名称2],并增强了抗氧化因子[具体抗氧化因子名称1]和[具体抗氧化因子名称2]。基于代谢组学分析,[该植物名称]蜂蜜提取物和三叶豆苷通过抑制铁死亡来调节UC的进展。机制上,它们提高了超氧化物歧化酶(SOD)水平和铁负荷,增加了谷胱甘肽(GSH)/氧化型谷胱甘肽(GSSG)比值,降低了丙二醛(MDA)含量和活性氧(ROS)释放,并上调了[具体信号通路名称]/[具体信号通路名称]途径,从而抑制DSS诱导的UC。此外,铁死亡相关基因的表达水平表明,它们降低了[具体基因名称1]、[具体基因名称2]和[具体基因名称3]的表达,同时增加了[具体基因名称4]的表达以抵抗铁死亡。总之,我们的研究发现,[该植物名称]蜂蜜通过激活[具体信号通路名称]/[具体信号通路名称]途径抑制铁死亡来改善DSS诱导的UC。这些发现进一步阐明了对[该植物名称]蜂蜜抗炎和抗氧化活性的理解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c9e/11351236/d96a22ac3985/antioxidants-13-00900-g001.jpg

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