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普拉蒂科登大花多糖抑制了感染PCV2的3D4/21细胞的炎症反应

Xiaocheng Guo¹, Ximan Zhao², Linjue Li²

¹College of Animal Science and Veterinary Medicine, Shandong Agricultural University, Tai`an, Shandong, 271018, China; Weifang University of Science and Technology, Weifang, Shandong, 262700, China.

Microbial pathogenesis

|February 29, 2024

概括

普拉提科登大花多糖 (PGPS) 有效地降低了猪肉病毒2型 (PCV2) 感染细胞的炎症. 它调节组织素乙化,抑制关键的炎症通路,提供一种潜在的治疗策略.

科学领域:

兽医免疫学兽医免疫学
分子生物学分子生物学
药理学药理学是指药理学的学科.

背景情况:

猪病毒2型 (PCV2) 感染会导致猪的多系统性炎症.
普拉提科登大花多糖 (PGPS) 已知具有免疫调节和抗病特性.
在3D4/21细胞中PCV2诱导的炎症中PGPS_t的确切作用和机制尚未完全理解.

研究的目的:

为了研究PGPS_t对PCV2感染的3D4/21细胞的抗炎作用.
在这种体外模型中阐明PGPS_t作用的潜在分子机制.

主要方法:

使用3D4/21细胞系建立PCV2诱导的细胞炎症模型.
用PGPS_t预处理细胞,然后对炎症标志物和信号通路进行分析.
使用的技术包括CCK-8,ELISA,qPCR,以及西布.

主要成果:

PGPS_t没有表现出毒性,并且保护PCV2感染的细胞免受炎症损伤.
PGPS抑制了素H3和H4的乙化,调节了HAT/HDAC活性,并降低了iNOS和COX-2的表达.
观察到促炎性细胞因子 (IL-1β,IL-6,TNF-α) 的显著减少和IL-10的促进.
PGPS抑制了p65,p38和Erk1/2的酸化,抑制了NF-κB的激活和促炎因子的表达.

结论:

在3D4/21细胞中,PGPS对PCV2诱导的炎症具有显著的抗炎作用.
机制包括调节组素乙化,减少炎症因子释放,减少促炎酶表达,并抑制NF-κB和MAPK信号通路.
这些发现为PGPS_t作为对抗PCV2相关炎症的潜在治疗剂提供了理论基础.

关键词:

基斯乙化基斯乙化炎症炎症是一种炎症.在PCV2中使用PCV2.这是一种Platycodon grandiflorus多糖化合物.

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