Glaesserella parasuis causes porcine Glässer's disease and lipopolysaccharide (LPS) induces acute inflammation and pathological damage. Baicalin has antioxidant, antimicrobial, and anti-inflammatory functions. Long noncoding RNAs (lncRNAs) play key regulatory functions during bacterial infection. However, the role of lncRNAs in the vascular dysfunction induced by a combination of G. parasuis and LPS during systemic inflammation and the effect of baicalin on lncRNA expression induced in porcine aortic vascular endothelial cells (PAVECs) by a combination of G. parasuis and LPS have not been investigated. In this study, we investigated the changes in lncRNA and mRNA expression induced in PAVECs by G. parasuis, LPS, or a combination of G. parasuis and LPS, and the action of baicalin on lncRNA expression induced in PAVECs by the combination of G. parasuis and LPS. Our results showed 133 lncRNAs and 602 genes were differentially expressed when PAVECs were stimulated with the combination of G. parasuis and LPS, whereas 107 lncRNAs and 936 genes were differentially expressed when PAVECs were stimulated with the combination of G. parasuis and LPS after pretreatment with baicalin. The Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis showed the dominant signaling pathways triggered by the combination of G. parasuis and LPS were the tumor necrosis factor signaling pathway, phosphatidylinositol signaling system, and inositol phosphate metabolism. Protein–protein interaction network analysis showed the differentially expressed target genes of the differentially expressed lncRNAs (DELs) were related to each other. A coexpression analysis indicated the expression levels of the DELs were co-regulated with those of their differentially expressed target genes. This is the first study to systematically compare the changes in lncRNAs and mRNAs in PAVECs stimulated with a combination of G. parasuis and LPS. Our data clarified the mechanisms underlying the vascular inflammation and damage triggered by G. parasuis and LPS, and it may provide novel targets for the treatment of LPS-induced systemic inflammation.

中文翻译：

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黄芩苷对副猪格拉斯菌与脂多糖联合诱导仔猪血管内皮细胞转录组变化的影响

Glaesserella parasuis引起猪格拉瑟氏病，脂多糖 (LPS) 引起急性炎症和病理损伤。黄芩苷具有抗氧化、抗菌和抗炎功能。长链非编码 RNA (lncRNA) 在细菌感染过程中发挥着关键的调节功能。然而，lncRNA 在全身炎症期间由副猪 G. parasuis和 LPS联合诱导的血管功能障碍中的作用以及黄芩苷对G. parasuis和 LPS联合诱导的猪主动脉血管内皮细胞 (PAVEC) 中 lncRNA 表达的影响没有被调查。在这项研究中，我们研究了副猪 G. parasuis 、LPS 或它们的组合在 PAVECs 中诱导的 lncRNA 和 mRNA 表达的变化。G. parasuis 和 LPS，以及黄芩苷对G. parasuis和 LPS联合诱导的 PAVECs 中 lncRNA 表达的作用。我们的结果表明，当 PAVECs 被副猪 G. parasuis 和 LPS联合刺激时，133 个 lncRNAs 和 602 个基因差异表达，而当 PAVECs 被G. parasuis和 LPS 预处理后，107 个 lncRNAs 和 936 个基因差异表达。黄芩苷。京都基因和基因组百科全书 (KEGG) 分析显示由G. parasuis组合触发的主要信号通路LPS 是肿瘤坏死因子信号通路、磷脂酰肌醇信号系统和磷酸肌醇代谢。蛋白质-蛋白质相互作用网络分析显示差异表达的lncRNA（DEL）的差异表达靶基因彼此相关。共表达分析表明 DEL 的表达水平与其差异表达的靶基因的表达水平共同调节。这是第一项系统地比较副猪 G. parasuis和 LPS组合刺激的 PAVEC 中 lncRNA 和 mRNA 变化的研究。我们的数据阐明了由副猪 G. parasuis引发的血管炎症和损伤的潜在机制 和 LPS，它可能为 LPS 诱导的全身炎症的治疗提供新的靶点。