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甜菜碱通过TLR4基因的表观遗传调控减轻脂多糖诱导的鸡骨骼肌炎症。

Betaine Alleviates LPS-Induced Chicken Skeletal Muscle Inflammation with the Epigenetic Modulation of the TLR4 Gene.

作者信息

Guo Feng, Jing Mengna, Zhang Aoyu, Yu Yan, Gao Pei, Wang Qiuxia, Wang Li, Xu Zhiyong, Ma Jinyou, Zhang Yanhong

机构信息

College of Animal Science and Veterinary Medicine, Henan Institute of Science and Technology, Xinxiang 453003, China.

出版信息

Animals (Basel). 2022 Jul 26;12(15):1899. doi: 10.3390/ani12151899.

DOI:10.3390/ani12151899
PMID:35892549
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9330308/
Abstract

Betaine was found to alleviate inflammation in different studies. Here, newly hatched broilers were randomly divided into control and betaine consumptive groups, who had access to normal drinking water and water with betaine at a dose of 1000 mg/L, respectively. At the age of two weeks, the boilers were intraperitoneally treated with LPS. The protective effects of betaine against LPS-induced skeletal muscle inflammation were studied. Betaine attenuated the LPS-induced overexpression of IL-6 significantly in the leg muscle. Furthermore, LPS lowered the expression of TLR4 and TLR2 but increased the expression of MyD88. Betaine eliminated the effect of LPS on the expression of TLR4 but not TLR2 and MyD88. LPS also increased the expression of Tet methylcytosine dioxygenase 2 (Tet2), and this effect was also eliminated by betaine consumption. MeDIP-qPCR analysis showed that the methylation level in the promoter region of IL-6 was decreased by LPS treatment, whilst betaine cannot prevent this effect. On the contrary, LPS significantly increase the methylation level in the promoter region of TLR4, which was decreased by the consumption of betaine. Our findings suggest that betaine can alleviate LPS-induced muscle inflammation in chicken, and the regulation of aberrant DNA methylation might be a possible mechanism.

摘要

在不同研究中发现甜菜碱可减轻炎症。在此,将新孵化的肉鸡随机分为对照组和甜菜碱消费组,分别提供正常饮用水和含1000 mg/L甜菜碱的水。两周龄时,对肉鸡进行腹腔注射脂多糖(LPS)处理。研究了甜菜碱对LPS诱导的骨骼肌炎症的保护作用。甜菜碱显著减轻了LPS诱导的腿部肌肉中白细胞介素-6(IL-6)的过度表达。此外,LPS降低了Toll样受体4(TLR4)和Toll样受体2(TLR2)的表达,但增加了髓样分化因子88(MyD88)的表达。甜菜碱消除了LPS对TLR4表达的影响,但对TLR2和MyD88的表达无此作用。LPS还增加了四氢甲基胞嘧啶双加氧酶2(Tet2)的表达,而食用甜菜碱也消除了这种作用。甲基化DNA免疫沉淀定量聚合酶链反应(MeDIP-qPCR)分析表明,LPS处理降低了IL-6启动子区域的甲基化水平,而甜菜碱无法阻止这种作用。相反,LPS显著增加了TLR4启动子区域的甲基化水平,而食用甜菜碱可降低该水平。我们的研究结果表明,甜菜碱可减轻LPS诱导的鸡肌肉炎症,异常DNA甲基化的调节可能是一种潜在机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e67/9330308/ffafd6cdcae8/animals-12-01899-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e67/9330308/93bb6fe3419b/animals-12-01899-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e67/9330308/d0cd41bb0c52/animals-12-01899-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e67/9330308/fe1e54819fb0/animals-12-01899-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e67/9330308/16393d575749/animals-12-01899-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e67/9330308/ffafd6cdcae8/animals-12-01899-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e67/9330308/93bb6fe3419b/animals-12-01899-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e67/9330308/d0cd41bb0c52/animals-12-01899-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e67/9330308/fe1e54819fb0/animals-12-01899-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e67/9330308/16393d575749/animals-12-01899-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0e67/9330308/ffafd6cdcae8/animals-12-01899-g005.jpg

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