Hydroxytyrosol Alleviates Intestinal Oxidative Stress by Regulating Bile Acid Metabolism in a Piglet Model

被引:0
作者
Wen, Xiaobin [1 ]
Wan, Fan [1 ]
Zhong, Ruqing [1 ]
Chen, Liang [1 ]
Zhang, Hongfu [1 ]
机构
[1] Chinese Acad Agr Sci, Inst Anim Sci, State Key Lab Anim Nutr & Feeding, Beijing 100193, Peoples R China
基金
中国国家自然科学基金;
关键词
hydroxytyrosol; gut microbiota; bile acid; intestinal health; oxidative stress; MITOCHONDRIAL BIOGENESIS; ACTIVATION; INJURY; NRF2; PROTECTS; CELLS; STIMULATION; INHIBITION; DAMAGE;
D O I
10.3390/ijms25115590
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Infants and young animals often suffer from intestinal damage caused by oxidative stress, which may adversely affect their overall health. Hydroxytyrosol, a plant polyphenol, has shown potential in decreasing intestinal oxidative stress, but its application and mechanism of action in infants and young animals are still inadequately documented. This study selected piglets as a model to investigate the alleviating effects of hydroxytyrosol on intestinal oxidative stress induced by diquat and its potential mechanism. Hydroxytyrosol improved intestinal morphology, characterized by higher villus height and villus height/crypt depth. Meanwhile, hydroxytyrosol led to higher expression of Occludin, MUC2, Nrf2, and its downstream genes, and lower expression of cytokines IL-1 beta, IL-6, and TNF-alpha. Both oxidative stress and hydroxytyrosol resulted in a higher abundance of Clostridium_sensu_stricto_1, and a lower abundance of Lactobacillus and Streptococcus, without a significant effect on short-chain fatty acids levels. Oxidative stress also led to disorders in bile acid (BA) metabolism, such as the lower levels of primary BAs, hyocholic acid, hyodeoxycholic acid, and tauroursodeoxycholic acid, which were partially restored by hydroxytyrosol. Correlation analysis revealed a positive correlation between these BA levels and the expression of Nrf2 and its downstream genes. Collectively, hydroxytyrosol may reduce oxidative stress-induced intestinal damage by regulating BA metabolism.
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页数:16
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