Porcine circovirus type 2 (PCV2) infection cause multi-systemic inflammation in pigs. polysaccharide (PGPS) has been reported to have the effects of immune regulation and disease resistance. Nevertheless, the role and mechanism of PGPS in the inflammatory response of 3D4/21 cells induced by PCV2 infection remain unclear. The present study aims to investigate effects of PGPS on inflammatory response and its possible underlying mechanisms in models. Cells were treated with PCV2 for 36 h to construct a cell inflammation model. The 3D4/21 cell lines were pretreated with or without PGPS, and the changes of inflammation-related markers and the signaling pathway were detected by CCK-8, ELISA, qPCR and Western blot. The results showed that PGPS was non-toxic to cells and protected PCV2-infected cells from inflammatory damage. PGPS could significantly inhibit the high acetylation of histone H3 (AcH3) and histone H4 (AcH4), down-regulate HAT and up-regulate HDAC activity, and reduce the expression of pro-inflammatory enzymes iNOS and COX-2 proteins levels. Then the levels of IL-1β, IL-6 and TNF-α were significantly inhibited, and the level of IL-10 was promoted. We also observed that PGPS inhibited the phosphorylation of p65, p38 and Erk1/2, which subsequently inhibited nuclear translocation of NF-κB p65 to express pro-inflammatory factors. In conclusion, PGPS can reduce the inflammatory response by regulating histone acetylation, reducing the release of inflammatory factors, reducing the expression of pro-inflammatory enzymes, and inhibiting the activation of NF-κB and MAPKs signaling pathways. This suggests that PGPS had an anti-inflammatory effect on the inflammatory response caused by PCV2 infection, which provided theoretical data support for the research.

中文翻译：

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桔梗多糖抑制PCV2感染3D4/21细胞的炎症反应

猪圆环病毒 2 型 (PCV2) 感染会引起猪的多系统炎症。据报道，多糖（PGPS）具有免疫调节和抗病作用。然而，PGPS在PCV2感染诱导的3D4/21细胞炎症反应中的作用和机制仍不清楚。本研究旨在探讨 PGPS 对模型炎症反应的影响及其可能的潜在机制。用PCV2处理细胞36小时，构建细胞炎症模型。用或不用PGPS预处理3D4/21细胞系，通过CCK-8、ELISA、qPCR和Western blot检测炎症相关标志物和信号通路的变化。结果表明，PGPS对细胞无毒，并能保护PCV2感染的细胞免受炎症损伤。PGPS可显着抑制组蛋白H3（AcH3）和组蛋白H4（AcH4）的高乙酰化，下调HAT并上调HDAC活性，降低促炎酶iNOS和COX-2蛋白的表达水平。IL-1β、IL-6、TNF-α水平明显受到抑制，IL-10水平升高。我们还观察到 PGPS 抑制 p65、p38 和 Erk1/2 的磷酸化，随后抑制 NF-κB p65 的核转位以表达促炎因子。总之，PGPS可以通过调节组蛋白乙酰化、减少炎症因子的释放、减少促炎酶的表达、抑制NF-κB和MAPKs信号通路的激活来减轻炎症反应。这表明PGPS对PCV2感染引起的炎症反应具有抗炎作用，为该研究提供了理论数据支持。