Ma Xia, Guo Zhenhuan, Zhang Zhiqiang, Li Xianghui, Liu Yonglu, Zhao Li, Wang Xuefei
College of Pharmaceutical Engineering, Henan University of Animal Husbandry and Economy, Zhengzhou 450046, China.
Department of Pharmacology, School of Pharmacy, Nanjing University of Chinese Medicine, Nanjing 210023, China.
Evid Based Complement Alternat Med. 2020 Apr 25;2020:3943672. doi: 10.1155/2020/3943672. eCollection 2020.
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)-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-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.
FA inhibited PPV infection-induced inflammasome activation as shown by decreases in the expression of NF-B, MyD88, and IL-6. FA also downregulated nonstructural (NS) 1 protein expression in infected PK-15 cells.
FA downregulated NS1 and TLR4 signaling, prevented the overproduction of reactive oxygen species, and suppressed the NF-B inflammasome axis to inhibit PPV-induced apoptosis in PK-15 cells.
猪细小病毒（PPV）感染诱导的细胞凋亡最近被确定为PPV诱导胎盘组织损伤导致繁殖失败的一个重要病理因素。在本研究中，我们证明了Toll样受体（TLR）4和核因子（NF）-κB炎性小体激活可能参与PPV感染诱导的细胞凋亡以及阿魏酸（FA）的保护潜力。PPV感染显著激活了TLR4、NF-κB、髓样分化因子88（MyD88）和白细胞介素（IL）-6的表达水平。然而，FA改善了病理过程，防止了组织学改变，并抑制了感染PPV的猪肾（PK-15）细胞的凋亡率。
如NF-κB、MyD88和IL-6表达的降低所示，FA抑制了PPV感染诱导的炎性小体激活。FA还下调了感染的PK-15细胞中非结构（NS）1蛋白的表达。
FA下调NS1和TLR4信号，防止活性氧的过量产生，并抑制NF-κB炎性小体轴，以抑制PPV诱导的PK-15细胞凋亡。
