食品科学 ›› 2025, Vol. 46 ›› Issue (5): 170-181.doi: 10.7506/spkx1002-6630-20240627-189

• 营养卫生 • 上一篇    下一篇

矢车菊素-3-葡萄糖苷通过调控肠道菌群改善自然衰老小鼠脑组织损伤

陈玉玉,彭文婷,宋歌,方微,綦文涛,王勇   

  1. (1.上海理工大学健康科学与工程学院,上海 200093;2.国家粮食和物资储备局科学研究院,北京 100037)
  • 出版日期:2025-03-15 发布日期:2025-02-07
  • 基金资助:
    “十四五”国家重点研发计划重点专项(2022YFF1100103);全国粮食和物资储备青年拔尖人才项目(QN2022401); 中央级公益性科研院所基本科研业务费专项(ZX2428)

Cyanidin-3-O-glucoside Ameliorates Brain Damage by Modulating Gut Microbiota in Naturally Aging Mice

CHEN Yuyu, PENG Wenting, SONG Ge, FANG Wei, QI Wentao, WANG Yong   

  1. (1. School of Health Science and Engineering, University of Shanghai for Science and Technology, Shanghai 200093, China; 2. Academy of National Food and Strategic Reserves Administration, Beijing 100037, China)
  • Online:2025-03-15 Published:2025-02-07

摘要: 目的:研究矢车菊素-3-葡萄糖苷(cyanidin-3-O-glucoside,C3G)对自然衰老小鼠脑组织损伤和肠道菌群的影响。方法:将2 月龄和18 月龄小鼠分为年轻对照组、年轻+C3G组、老年模型组和老年+C3G组,以50 mg/kg剂量的C3G连续灌胃8 周。分别测定血清中炎症因子和抗氧化指标、脑组织中神经营养因子和脑损伤相关标志物的表达量、肠道内容物中微生物多样性以及代谢产物变化。结果:C3G可显著降低老年小鼠的炎症因子水平(P<0.05),增加抗氧化酶活性(P<0.05),上调脑源性神经营养因子的表达,抑制β-淀粉样蛋白(1-42)等脑损伤标志物的产生(P<0.05)。此外,C3G增加了肠道中粪杆菌属(Faecalibaculum)和双歧杆菌属(Bifidobacterium)的相对丰度,降低了肠杆菌属(Enterorhabdus)的相对丰度;同时肠道菌群的变化促使二十二碳六烯酸和二十碳五烯酸含量增加,亚油酸含量减少(P<0.05)。进一步的相关性分析表明,粪杆菌属和双歧杆菌属与炎症因子和神经损伤相关指标呈负相关,与抗氧化能力和神经营养因子呈正相关。结论:C3G可通过调控肠道菌群组成缓解衰老相关神经损伤,改善自然衰老小鼠的脑健康。本研究结果可为利用花色苷开发具有延缓衰老功能的健康食品提供理论基础。

关键词: 矢车菊素-3-葡萄糖苷;自然衰老;脑损伤;神经炎症;肠道菌群;代谢产物

Abstract: Objective: To investigate the effect of cyanidin-3-O-glucoside (C3G) on brain damage and gut microbiota in naturally aging mice. Methods: Mice aged 2 and 18 months were divided into four groups: young control, young + C3G, aging model and aged + C3G. The second and fourth groups were administered by gavage with 50 mg/kg C3G consecutively for eight weeks. The following parameters were assessed: serum levels of inflammatory factors and antioxidant indexes, expression levels of neurotrophic factors and brain damage markers in brain tissue; microbial diversity and metabolite changes in intestinal contents. Results: C3G significantly decreased the level of inflammatory factors (P < 0.05), increased the activity of antioxidant enzymes (P < 0.05), and up-regulated the expression of brain-derived neurotrophic factor (BDNF), while inhibiting the production of brain damage markers including beta amyloid 1-42 (Aβ1-42) (P < 0.05). In addition, C3G increased the relative abundance of Faecalibaculum and Bifidobacterium in the gut, while decreasing the level of Enterorhabdus. These changes in gut microbiota contributed to the production of docosahexaenoic acid and eicosapentaenoic acid and decreased linoleic acid levels (P < 0.05). Correlation analysis showed that Faecalibaculum and Bifidobacterium were negatively correlated with inflammatory factors and nerve damage indicators, but positively correlated with antioxidant capacity and neurotrophic factors. Conclusion: C3G can alleviate aging-related neurological damage and improve brain health in naturally aging mice by modulating gut microbiota. This finding may provide a theoretical basis for the development of aging-delaying health foods containing anthocyanins.

Key words: cyanidin-3-O-glucoside; natural aging; brain damage; neuroinflammation; gut microbiota; metabolites

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