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膳食橙皮苷可抑制雄性小鼠中脂多糖诱导的炎症。

Dietary Hesperidin Suppresses Lipopolysaccharide-Induced Inflammation in Male Mice.

作者信息

Sato Mizuho, Okuno Alato, Ishisono Keita, Yajima Yuhei, Toyoda Atsushi

机构信息

College of Agriculture, Ibaraki University, Ami, Ibaraki, Japan.

United Graduate School of Agricultural Science, Tokyo University of Agriculture and Technology, Fuchu, Tokyo, Japan.

出版信息

Int J Tryptophan Res. 2022 Oct 28;15:11786469221128697. doi: 10.1177/11786469221128697. eCollection 2022.

DOI:10.1177/11786469221128697
PMID:36325028
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9619875/
Abstract

Depressive disorders are partially attributed to chronic inflammation associated with the tryptophan (Trp)-kynurenine (Kyn) pathway. Recent evidence suggests that anti-inflammatory agents may reduce the risk of depression. The present study aimed to elucidate the potential of the citrus flavonoid hesperidin, which exhibits anti-inflammatory activity, in suppressing the Trp-Kyn pathway in the brain, using a lipopolysaccharide (LPS)-induced inflammation mouse model. Dietary hesperidin was found to suppress activation of the Trp-Kyn pathway in the prefrontal cortex. In addition, it reduced systemic LPS-induced signs of illness, such as low skin temperature and enhanced leukocyte count in the blood. However, dietary supplementation with hesperidin did not improve body weight loss, food intake, water intake, or splenic increases in leukocyte numbers in the LPS model. Collectively, the results suggest that dietary hesperidin can partially regulate central and peripheral events linked to inflammation in LPS mouse models.

摘要

抑郁症部分归因于与色氨酸(Trp)-犬尿氨酸(Kyn)途径相关的慢性炎症。最近的证据表明,抗炎药物可能会降低患抑郁症的风险。本研究旨在利用脂多糖(LPS)诱导的炎症小鼠模型,阐明具有抗炎活性的柑橘类黄酮橙皮苷在抑制大脑中Trp-Kyn途径方面的潜力。研究发现,饮食中的橙皮苷可抑制前额叶皮质中Trp-Kyn途径的激活。此外,它还减轻了全身性LPS诱导的疾病症状,如皮肤温度降低和血液中白细胞计数增加。然而,在LPS模型中,饮食补充橙皮苷并未改善体重减轻、食物摄入量、饮水量或脾脏白细胞数量增加的情况。总体而言,结果表明饮食中的橙皮苷可以部分调节LPS小鼠模型中与炎症相关的中枢和外周事件。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/330b/9619875/41945b0e487f/10.1177_11786469221128697-fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/330b/9619875/ab6d8a1ca0c6/10.1177_11786469221128697-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/330b/9619875/b0f9f6788415/10.1177_11786469221128697-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/330b/9619875/7e134c8b55e1/10.1177_11786469221128697-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/330b/9619875/5f4cf1c6c859/10.1177_11786469221128697-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/330b/9619875/41945b0e487f/10.1177_11786469221128697-fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/330b/9619875/ab6d8a1ca0c6/10.1177_11786469221128697-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/330b/9619875/b0f9f6788415/10.1177_11786469221128697-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/330b/9619875/7e134c8b55e1/10.1177_11786469221128697-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/330b/9619875/5f4cf1c6c859/10.1177_11786469221128697-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/330b/9619875/41945b0e487f/10.1177_11786469221128697-fig5.jpg

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