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Selenomethionine alleviates LPS-induced chicken myocardial inflammation by regulating the miR-128-3p-p38 MAPK axis and oxidative stress.
Metallomics ( IF 2.9 ) Pub Date : 2019-11-06 , DOI: 10.1039/c9mt00216b Jing Liu 1 , Shengchen Wang , Qiaojian Zhang , Xiaojing Li , Shiwen Xu
Metallomics ( IF 2.9 ) Pub Date : 2019-11-06 , DOI: 10.1039/c9mt00216b Jing Liu 1 , Shengchen Wang , Qiaojian Zhang , Xiaojing Li , Shiwen Xu
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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-κB 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-κB, while the expression of TNF-α, IL-1, PTGE, COX-2 and iNOS increased. Additionally, the expression of IL-4 and IL-6 increased and IFN-γ 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-κB pathway.
中文翻译：
硒代蛋氨酸通过调节miR-128-3p-p38 MAPK轴和氧化应激减轻LPS诱导的鸡心肌炎。
硒与心脏病的发生密切相关，适量的硒可以缓解各种因素引起的炎症变化。脂多糖（LPS）作为革兰氏阴性细菌细胞壁的特定成分，通常用于构建各种炎症模型。为了探讨硒对LPS诱导的鸡心肌炎症的影响，我们选择了4个月大的蛋鸡饲喂含0.5 g kg -1的富硒饮食硒，并在8个月大时将LPS注入腹腔以建立炎症模型。我们通过光学显微镜观察了心肌组织病变，并通过qRT-PCR和Western blot检测了miR-128-3p，p38MAPK和NF-κB通路相关的炎症因子和Th1 / Th2相关因子。结果表明，LPS刺激抑制了miR-128-3p，增加了p38MAPK和NF-κB的表达，同时增加了TNF-α，IL-1，PTGE，COX-2和iNOS的表达。此外，IL-4和IL-6的表达增加而IFN-γ减少，表明Th1 / Th2失衡。我们还发现，LPS处理不仅增加了H 2 O 2的含量心肌中的MDA和MDA，也使HSP60，HSP70和HSP90的表达增加，而SOD，GPX和CAT的活性以及GSH的含量下降。有趣的是，添加硒可以减轻上述指标的变化。最后，我们得出结论，硒抑制了氧化应激的发生，并最终通过miR-128-3p-p38MAPK-NF-κB途径减轻了LPS诱导的心肌炎症。
更新日期：2019-11-06
中文翻译：
硒代蛋氨酸通过调节miR-128-3p-p38 MAPK轴和氧化应激减轻LPS诱导的鸡心肌炎。
硒与心脏病的发生密切相关，适量的硒可以缓解各种因素引起的炎症变化。脂多糖（LPS）作为革兰氏阴性细菌细胞壁的特定成分，通常用于构建各种炎症模型。为了探讨硒对LPS诱导的鸡心肌炎症的影响，我们选择了4个月大的蛋鸡饲喂含0.5 g kg -1的富硒饮食硒，并在8个月大时将LPS注入腹腔以建立炎症模型。我们通过光学显微镜观察了心肌组织病变，并通过qRT-PCR和Western blot检测了miR-128-3p，p38MAPK和NF-κB通路相关的炎症因子和Th1 / Th2相关因子。结果表明，LPS刺激抑制了miR-128-3p，增加了p38MAPK和NF-κB的表达，同时增加了TNF-α，IL-1，PTGE，COX-2和iNOS的表达。此外，IL-4和IL-6的表达增加而IFN-γ减少，表明Th1 / Th2失衡。我们还发现，LPS处理不仅增加了H 2 O 2的含量心肌中的MDA和MDA，也使HSP60，HSP70和HSP90的表达增加，而SOD，GPX和CAT的活性以及GSH的含量下降。有趣的是，添加硒可以减轻上述指标的变化。最后，我们得出结论，硒抑制了氧化应激的发生，并最终通过miR-128-3p-p38MAPK-NF-κB途径减轻了LPS诱导的心肌炎症。
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