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通过DNMT3a/SIRT1介导的表观遗传调制改善肥胖

Mi Liu^1,2, Haizhi Li³, Jingzhi Zhang¹

¹School of Public Health, The Key Laboratory of Environmental Pollution Monitoring and Disease Control, Ministry of Education Guizhou Medical University Guiyang China.

Food science & nutrition

|September 5, 2025

概括

Rosa roxburghii Tratt发酵 (RRTFB) 通过通过DNMT3a/SIRT1途径调节DNA甲基化来对抗肥胖. 这种由黄驱动的植物化疗策略可以减少肥胖大鼠的炎症和氧化应激.

科学领域:

表观遗传学和营养药
分子生物学和生物化学
肥胖研究

背景情况:

肥胖并发症源于慢性炎症和氧化应激, 常常由异常的DNA甲基化加剧.
因为天然产品具有抗炎和抗氧化作用,

研究的目的:

研究罗莎·罗克斯堡希·特拉特发酵 (RRTFB) 在肥胖症中的分子机制.
确定RRTFB的活性成分并评估其治疗价值.
探索RRTFB对DNA甲基化和相关途径的影响.

主要方法:

在Sprague-Dawley大鼠中,高脂肪饮食 (HFD) 诱导肥胖,RRTFB干预.
用于甲基化分析的减少表示二硫酸盐测序 (RRBS).
分子对接,表面等离子体共振 (SPR) 和生物化学测试以确定活性成分和验证目标.

主要成果:

在肥胖大鼠中,RRTFB显著降低了炎症标志物 (IL-6,TNF-α),氧化应激 (MDA) 和DNMT3a水平,同时增加了抗氧化酶 (SOD,GSH- pX,CAT).
在与脂肪代谢,氧化应激和炎症相关的基因中,RRBS确定了差异性甲基化区域.
通过与DNMT3a结合的类化合物,RRTFB降低了SIRT1促进物甲基化和增加了SIRT1表达.

结论:

通过DNMT3a/SIRT1介导的表观遗传调节,RRTFB可以减轻肥胖.
黄被认为是RRTFB有效性的主要生物活性成分.
RRTFB显示出作为肥胖管理的植物化疗剂的潜力.

关键词:

DNA 甲基化罗莎·罗克斯堡·特拉特的发酵一个SIRT1 抗氧化剂肥胖问题

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