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Gallic acid mitigates LPS-induced inflammatory response via suppressing NF-κB signalling pathway in IPEC-J2 cells
Journal of Animal Physiology and Animal Nutrition ( IF 2.7 ) Pub Date : 2021-07-20 , DOI: 10.1111/jpn.13612
Long Cai 1 , Zixi Wei 1 , Xuemei Zhao 1 , Yanpin Li 1 , Xilong Li 1 , Xianren Jiang 1
Affiliation  

Gallic acid is a phenolic compound that exhibits antibacterial, antioxidative and anti-inflammatory functions. In a previous study, we found that dietary supplementation with gallic acid decreased incidence of diarrhoea and protected intestinal integrity in weaning piglets. However, the underlying mechanism remains unclear. Here, a pig intestinal epithelial cell line (IPEC-J2) was used as an in vitro model to explore the antioxidant and anti-inflammatory capacity of gallic acid. IPEC-J2 cells were stimulated with hydrogen peroxide (H2O2) and lipopolysaccharide (LPS) to establish oxidative and inflammatory models, respectively. Results showed that H2O2 significantly decreased catalase (CAT) secretion and CAT mRNA abundance in the cells (p < 0.05), while pretreatment with gallic acid did not prevent the decrease in CAT expression induced by H2O2. However, gallic acid pretreatment mitigated the increased expression of the tumour necrosis factor-α and interleukin-8 genes caused by LPS in IPEC-J2 cells (p < 0.05). In addition, pretreatment with gallic acid significantly suppressed phosphorylation of NF-κB and IκBα in LPS-stimulated IPEC-J2 cells. Moreover, LPS stimulation decreased the protein abundance of zona occludens 1 (ZO-1) and occludin, while pretreatment with gallic acid preserved expression level of tight junction proteins ZO-1 and occludin in LPS-stimulated IPEC-J2 cells (p < 0.05). In conclusion, gallic acid may mitigate LPS-induced inflammatory responses by inhibiting the NF-κB signalling pathway, exerting positive effects on the barrier function of IPEC-J2 cells.

中文翻译:

没食子酸通过抑制 IPEC-J2 细胞中的 NF-κB 信号通路减轻 LPS 诱导的炎症反应

没食子酸是一种酚类化合物,具有抗菌、抗氧化和抗炎功能。在之前的一项研究中,我们发现在日粮中添加没食子酸可降低断奶仔猪腹泻的发生率并保护肠道完整性。然而,潜在的机制仍不清楚。在这里,猪肠上皮细胞系(IPEC-J2)被用作体外模型来探索没食子酸的抗氧化和抗炎能力。用过氧化氢(H 2 O 2)和脂多糖(LPS)刺激IPEC-J2细胞分别建立氧化和炎症模型。结果表明,H 2 O 2显着降低细胞中的过氧化氢酶 (CAT) 分泌和 CAT mRNA 丰度 ( p  < 0.05),而没食子酸预处理并未阻止 H 2 O 2诱导的 CAT 表达降低。然而,没食子酸预处理减轻了LPS引起的IPEC-J2细胞中肿瘤坏死因子-α和白细胞介素8基因的表达增加(p  < 0.05)。此外,没食子酸预处理显着抑制了 LPS 刺激的 IPEC-J2 细胞中 NF-κB 和 IκBα 的磷酸化。此外,LPS 刺激降低了 zona occludens 1 (ZO-1) 和 occludin 的蛋白质丰度,而没食子酸预处理保留了 LPS 刺激的 IPEC-J2 细胞中紧密连接蛋白 ZO-1 和 occludin 的表达水平。p  < 0.05)。总之,没食子酸可通过抑制 NF-κB 信号通路减轻 LPS 诱导的炎症反应,对 IPEC-J2 细胞的屏障功能发挥积极作用。
更新日期:2021-07-20
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