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姜和 6-姜酚可预防脂多糖诱导的小鼠肠道屏障损伤和肝损伤。

Ginger and 6-gingerol prevent lipopolysaccharide-induced intestinal barrier damage and liver injury in mice.

机构信息

Institute of Quality Standard and Testing Technology for Agro-products, Chinese Academy of Agricultural Sciences, Beijing, China.

College of Food Science and Nutritional Engineering, China Agricultural University, Beijing, China.

出版信息

J Sci Food Agric. 2022 Feb;102(3):1066-1075. doi: 10.1002/jsfa.11442. Epub 2021 Aug 11.

DOI:10.1002/jsfa.11442
PMID:34309869
Abstract

BACKGROUND

Inflammation-related diseases present a significant public health problem. Ginger is a flavoring spice and medicinal herb with anti-inflammatory activity. This study investigated the preventive effects of ginger extract (GE) and its main bioactive component, 6-gingerol (6G), on lipopolysaccharide (LPS)-induced intestinal barrier dysfunction and liver injury in mice.

RESULTS

GE and 6G were orally administered to mice for seven consecutive days before LPS administration. After 24 h, the mice were sacrificed. GE and 6G were found to significantly reverse LPS-induced inflammation in the mouse ileum by modifying the NF-κB pathway. They also alleviated apoptosis in the ileum by downregulating Bax and cytochrome c gene expression and by inhibiting the caspase-3 pathway. Through the aforementioned mechanisms, GE and 6G restored the intestinal barrier by increasing ZO-1 and claudin-1 protein expressions. Gut-derived LPS induced inflammation and apoptosis in the liver; these effects were markedly reversed through GE and 6G treatment. 6G was the most abundant component in GE, as evidenced through liquid chromatography-mass spectrometry, and accounted for >50% of total gingerols and shogaols in GE.

CONCLUSION

The current results support the use of GE and 6G as dietary supplements to protect against gut-derived endotoxemia-associated inflammatory response and disorders. © 2021 Society of Chemical Industry.

摘要

背景

炎症相关疾病是一个重大的公共卫生问题。生姜既是一种调味品,也是一种具有抗炎活性的药用草本植物。本研究旨在探讨生姜提取物(GE)及其主要生物活性成分 6-姜酚(6G)对脂多糖(LPS)诱导的小鼠肠道屏障功能障碍和肝损伤的预防作用。

结果

在 LPS 给药前连续 7 天对小鼠进行 GE 和 6G 口服给药。24 小时后处死小鼠。研究发现,GE 和 6G 通过调节 NF-κB 通路,显著逆转 LPS 诱导的小鼠回肠炎症。它们还通过下调 Bax 和细胞色素 c 基因表达和抑制 caspase-3 通路来减轻回肠细胞凋亡。通过上述机制,GE 和 6G 通过增加 ZO-1 和闭合蛋白-1 蛋白表达来恢复肠道屏障。肠道来源的 LPS 诱导肝脏炎症和细胞凋亡;通过 GE 和 6G 治疗可显著逆转这些作用。通过液相色谱-质谱法发现,6G 是 GE 中最丰富的成分,占 GE 中总姜酚和姜烯酚的>50%。

结论

目前的结果支持将 GE 和 6G 用作膳食补充剂,以预防肠道来源的内毒素血症相关炎症反应和紊乱。© 2021 化学工业协会。

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