Ferulic Acid Protects against Porcine Parvovirus Infection-Induced Apoptosis by Suppressing the Nuclear Factor-κB Inflammasome Axis and Toll-Like Receptor 4 via Nonstructural Protein 1
Ferulic Acid Protects against Porcine Parvovirus Infection-Induced Apoptosis by Suppressing the Nuclear Factor-κB Inflammasome Axis and Toll-Like Receptor 4 via Nonstructural Protein 1
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DOI：
10.1155/2020/3943672
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发表时间：
2020-04-26
影响因子：
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通讯作者：
Wang, Xuefei
中科院分区：
文献类型：
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作者：
Ma, Xia;Guo, Zhenhuan;Wang, Xuefei
背景猪细小病毒（PPV）感染引起的胎盘细胞凋亡是PPV引起胎盘组织损伤，导致繁殖失败的重要病理因素。在本研究中，我们证明了Toll样受体（TLR）4和核因子（NF）-κ B炎性小体激活可能参与PPV感染诱导的细胞凋亡和阿魏酸（FA）的保护潜力。PPV感染显著激活了TLR 4、NF-κ B、MyD 88和白细胞介素（IL）-6的表达水平。然而，FA可改善PPV感染的猪肾（PK-15）细胞的病理过程，防止组织学改变，并抑制细胞凋亡率。结果FA抑制PPV感染诱导的炎性小体活化，如NF-κ B、MyD 88和IL-6表达降低所示。FA也下调非结构（NS）1蛋白在感染的PK-15细胞的表达。结论. FA下调NS 1和TLR 4信号，防止活性氧的过度产生，并抑制NF-κ B炎性体轴，以抑制PPV诱导的PK-15细胞凋亡。
Background. Porcine parvovirus (PPV) infection-induced apoptosis was recently identified as an important pathological factor in PPV-induced placental tissue damage, resulting in reproduction failure. In the present study, we demonstrate the possible involvement of toll-like receptor (TLR) 4 and nuclear factor (NF)-kappa B inflammasome activation in PPV infection-induced apoptosis and the protective potential of ferulic acid (FA). PPV infection significantly activated the expression levels of TLR4, NF-kappa B, MyD88, and interleukin (IL)-6. However, FA ameliorated the pathological process, prevented histological alterations, and inhibited the apoptosis rate in porcine kidney (PK-15) cells infected with PPV. Results. FA inhibited PPV infection-induced inflammasome activation as shown by decreases in the expression of NF-kappa B, MyD88, and IL-6. FA also downregulated nonstructural (NS) 1 protein expression in infected PK-15 cells. Conclusions. FA downregulated NS1 and TLR4 signaling, prevented the overproduction of reactive oxygen species, and suppressed the NF-kappa B inflammasome axis to inhibit PPV-induced apoptosis in PK-15 cells.