Selenomethionine alleviates LPS-induced chicken myocardial inflammation by regulating the miR-128-3p-p38 MAPK axis and oxidative stress

被引:0
|
作者
Liu, Jing [1 ]
Wang, Shengchen [1 ]
Zhang, Qiaojian [1 ]
Li, Xiaojing [1 ]
Xu, Shiwen [1 ]
机构
[1] Northeast Agr Univ, Coll Vet Med, Harbin 150030, Peoples R China
基金
中国国家自然科学基金;
关键词
ACTIVATED PROTEIN-KINASE; TH1/TH2; IMBALANCE; SELENIUM; APOPTOSIS; PATHWAY; EXPRESSION; DAMAGE; MODULATION; INJURY; CELLS;
D O I
10.1039/c9mt00216b
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
Selenium is closely related to the occurrence of heart disease, and an appropriate amount of selenium can alleviate inflammatory changes caused by various factors. Lipopolysaccharide (LPS), as a specific component of the cell wall of Gram-negative bacteria, is often used to construct various inflammatory models. In order to explore the effect of selenium on LPS-induced myocardial inflammation in chickens, we chose 4-month-old laying hens to be fed with a selenium-rich diet containing 0.5 g kg(-1) Se, and injected LPS into the abdominal cavity at the age of 8 months to establish an inflammation model. We observed the myocardial tissue lesions by light microscopy, and detected miR-128-3p, p38MAPK, and NF-kappa B pathway-associated inflammatory factors and Th1/Th2 related factors by qRT-PCR and Western blot. The results showed that LPS stimulation inhibited miR-128-3p, which increased the expression of p38MAPK and NF-kappa B, while the expression of TNF-alpha, IL-1, PTGE, COX-2 and iNOS increased. Additionally, the expression of IL-4 and IL-6 increased and IFN-gamma decreased, suggesting an imbalance of Th1/Th2. We also found that LPS treatment not only increased the content of H2O2 and MDA in the myocardium, but also increased the expression of HSP60, HSP70 and HSP90, while the activity of SOD, GPX and CAT and the content of GSH decreased. Interestingly, the addition of selenium can alleviate the changes in the above indicators. Finally, we concluded that selenium inhibits the occurrence of oxidative stress and ultimately alleviates myocardial inflammation induced by LPS through the miR-128-3p-p38MAPK-NF-kappa B pathway.
引用
收藏
页码:54 / 64
页数:11
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