Flavonoids from Seabuckthorn ( L.) restore CUMS-induced depressive disorder and regulate the gut microbiota in mice

• Published in: Food & function Vol. 14; no. 16; pp. 7426 - 7438
• Main Authors: Xia, Chen-Xi, Gao, Alex Xiong, Zhu, Yue, Dong, Tina Ting-Xia, Tsim, Karl Wah-Keung
• Format: Journal Article
• Language: English
• Published: England Royal Society of Chemistry 14.08.2023
• Subjects: Dietary supplements; Flavonoids; Health risks; Hippophae rhamnoides; Homology; Hormones; Intestinal microflora; Kaempferol; Mental depression; Mental disorders; Microbiota; Microorganisms; Natural & organic foods; Neurotrophic factors; Quercetin; Signs and symptoms
• ISSN: 2042-6496; 2042-650X
• DOI: 10.1039/d3fo01332d

Seabuckthorn ( Hippophae rhamnoides L.), which is enriched with flavonoids, including isorhamnetin, quercetin and kaempferol, is a representative example of "medicine food homology" targeting several diseases. Major depressive disorders seriously threaten mental health worldwide and may even lead to death. Chronic unpredictable mild stress (CUMS)-induced depressive-like symptoms in mice are usually considered as the highest similarity to the situation in humans. Herein, we determined the potential functions of the flavonoid-enriched fraction from Seabuckthorn, which was named SBF, in treating major depressive disorder in mice. In the CUMS-induced mouse model, the intake of SBF reversed their depressive behaviors and relieved the CUMS-disturbed levels of neurotrophins, neurotransmitters, stress-related hormones, and inflammation-related cytokines. Additionally, the treatment of depressive mice with SBF showed ability to regulate the gut microbiota, especially in decreasing the abundance of Lactobacillaceae , while increasing the abundance of Lachnospiraceae at the family level. The results suggest the beneficial effects of Seabuckthorn flavonoids in functioning as a health food supplement to treat major depressive disorders. Seabuckthorn flavonoids mitigated depressive behaviors, improved biochemical indexes and modulated the gut microbiota of CUMS-induced mice.