中国神经再生研究(英文版) ›› 2026, Vol. 21 ›› Issue (1): 324-332.doi: 10.4103/NRR.NRR-D-23-02039

• 原著:神经损伤修复保护与再生 • 上一篇    下一篇

仙人掌刺梨果实甜菜黄素对高脂饮食引起神经元损伤和肠道微生物群失调具有积极影响

  

  • 出版日期:2026-01-15 发布日期:2025-04-24

Positive impact of indicaxanthin from Opuntia ficusindica fruit on high-fat diet–induced neuronal damage and gut microbiota dysbiosis

Simona Terzo1 , Antonella Amato1, 2, *, Pasquale Calvi1, 3, Marta Giardina1 , Domenico Nuzzo2 , Pasquale Picone2 , Antonio Palumbo-Piccionello1 , Sara Amata1 , Ilenia Concetta Giardina1 , Alessandro Massaro1 , Ignazio Restivo1 , Alessandro Attanzio1 , Luisa Tesoriere1 , Mario Allegra1 , Flavia Mulè1, *   

  1. 1 Department of Biological- Chemical- Pharmaceutical Science and Technology, University of Palermo, Palermo, Italy;  2 Institute for Biomedical Research and Innovation – IRIB, Palermo, Italy;  3 Department of Biomedicine, Neuroscience and Advanced Diagnostic, University of Palermo, Palermo, Italy
  • Online:2026-01-15 Published:2025-04-24
  • Contact: Flavia Mulè, flavia.mule@unipa.it; Antonella Amato, antonella.amato@unipa.it.

摘要:

甜菜黄素(Indicaxanthin,Ind)具有抗氧化和消炎作用;然而,Ind 的神经保护潜力知之甚少。为了解甜菜黄素对高脂饮食(HFD)诱导的小鼠神经元损伤和肠道微生物群失调的影响,实验分别给予小鼠以14周的标准饮食喂养和高脂饮食喂养。以高脂饮食喂养的最后4周喂服甜菜黄素(0.86mg/kg/d)。结果发现,甜菜黄素通过下调脑组织促凋亡基因和增加抗凋亡基因的表达,减少了神经元凋亡,还能显著降低神经炎症蛋白和基因的表达,并通过降低活性氧和氮、丙二醛和一氧化氮(NO)水平来抑制高脂饮食诱导的神经元氧化应激。同时,甜菜黄素还通过增加肠道健康细菌属毛螺菌、拟普雷沃氏菌和乳杆菌的丰度,减少与不健康特征相关的细菌厌氧菌、粪杆菌、罗姆布茨菌和嗜胆菌,改善了微生物菌群的组成。总之,甜菜黄素对高脂饮食诱导的肥胖小鼠神经元损伤和肠道微微生物菌群有积极的影响。

https://orcid.org/0000-0003-0676-0142 (Flavia Mulè); https://orcid.org/0000-0002-3343-9656 (Antonella Amato)

关键词: 肠道微生物群失调, 高脂饮食, 吲哚黄质, 微生物群, 神经元凋亡, 神经变性, 神经炎症, 肥胖症, 仙人掌刺梨

Abstract: Indicaxanthin is a betalain that is abundant in Opuntia ficus-indica orange fruit and has antioxidative and anti-inflammatory effects. Nevertheless, very little is known about the neuroprotective potential of indicaxanthin. This study investigated the impact of indicaxanthin on neuronal damage and gut microbiota dysbiosis induced by a high-fat diet in mice. The mice were divided into three groups according to different diets: the negative control group was fed a standard diet; the high-fat diet group was fed a high-fat diet; and the high-fat diet + indicaxanthin group was fed a high-fat diet and received indicaxanthin orally (0.86 mg/kg per day) for 4 weeks. Brain apoptosis, redox status, inflammation, and the gut microbiota composition were compared among the different animal groups. The results demonstrated that indicaxanthin treatment reduced neuronal apoptosis by downregulating the expression of proapoptotic genes and increasing the expression of antiapoptotic genes. Indicaxanthin also markedly decreased the expression of neuroinflammatory proteins and genes and inhibited high-fat diet–induced neuronal oxidative stress by reducing reactive oxygen and nitrogen species, malondialdehyde, and nitric oxide levels. In addition, indicaxanthin treatment improved the microflora composition by increasing the abundance of healthy bacterial genera, known as producers of short-chain fatty acids (Lachnospiraceae, Alloprovetella, and Lactobacillus), and by reducing bacteria related to unhealthy profiles (Blautia, Faecalibaculum, Romboutsia and Bilophila). In conclusion, indicaxanthin has a positive effect on high-fat diet–induced neuronal damage and on the gut microbiota composition in obese mice.

Key words: gut microbiota dysbiosis, high-fat diet, indicaxanthin, microflora, neuronal apoptosis, neurodegeneration, neuroinflammation, obesity, Opuntia ficus-indica fruit