阿魏酸通过非结构蛋白1抑制核因子-κB炎性小体轴和Toll样受体4，从而抵御猪细小病毒感染诱导的细胞凋亡。

Ferulic Acid Protects against Porcine Parvovirus Infection-Induced Apoptosis by Suppressing the Nuclear Factor-B Inflammasome Axis and Toll-Like Receptor 4 via Nonstructural Protein 1.

作者信息

Ma Xia, Guo Zhenhuan, Zhang Zhiqiang, Li Xianghui, Liu Yonglu, Zhao Li, Wang Xuefei

机构信息

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.

出版信息

Evid Based Complement Alternat Med. 2020 Apr 25;2020:3943672. doi: 10.1155/2020/3943672. eCollection 2020.

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)-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.

RESULTS

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.

CONCLUSIONS

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.

背景

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。