Abstract
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)-κB 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-κB, 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-κB, 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-κB inflammasome axis to inhibit PPV-induced apoptosis in PK-15 cells.
Highlights
Porcine parvovirus (PPV) infection has been acknowledged as a primary cause of reproductive disorders in pregnant cows
Monoclonal antibodies against nuclear factor (NF)-κB, tumor necrosis factor receptor-associated factor (TRAF) 6, IκB kinase (IKK) α, MyD88, c-jun N-terminal kinase (JNK), and β-actin were purchased from Cell Signaling Technology (Shanghai, China). e DMEM medium and fetal bovine serum (FBS) were from Gibco BRL (Grand Island, NY, USA). e FITC annexin V Apoptosis Detection Kit was TM from BD Biosciences (San Jose, CA, USA)
PPV infection is known to induce apoptosis in PK-15 cells, and we previously found that this could be inhibited by ferulic acid (FA) [1, 2]
Summary
Porcine parvovirus (PPV) infection has been acknowledged as a primary cause of reproductive disorders in pregnant cows. It is a crucial causative agent of diarrhea, skin disease, and arthritis in swine [1, 2]. 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-κB, MyD88, and IL-6. FA downregulated NS1 and TLR4 signaling, prevented the overproduction of reactive oxygen species, and suppressed the NF-κB inflammasome axis to inhibit PPV-induced apoptosis in PK-15 cells
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