Your browser doesn't support javascript.
Glycyrrhizin Inhibits PEDV Infection and Proinflammatory Cytokine Secretion via the HMGB1/TLR4-MAPK p38 Pathway.
Gao, Ruyi; Zhang, Yongshuai; Kang, Yuhui; Xu, Weiyin; Jiang, Luyao; Guo, Tingting; Huan, Changchao.
  • Gao R; Institutes of Agricultural Science and Technology Development, College of Veterinary Medicine, Yangzhou University, Yangzhou 225009, China.
  • Zhang Y; Jiangsu Co-Innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, Yangzhou 225009, China.
  • Kang Y; Key Laboratory of Avian Bioproduct Development, Ministry of Agriculture and Rural Affairs, Yangzhou 225009, China.
  • Xu W; Institutes of Agricultural Science and Technology Development, College of Veterinary Medicine, Yangzhou University, Yangzhou 225009, China.
  • Jiang L; Jiangsu Co-Innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, Yangzhou 225009, China.
  • Guo T; Key Laboratory of Avian Bioproduct Development, Ministry of Agriculture and Rural Affairs, Yangzhou 225009, China.
  • Huan C; Institutes of Agricultural Science and Technology Development, College of Veterinary Medicine, Yangzhou University, Yangzhou 225009, China.
Int J Mol Sci ; 21(8)2020 Apr 23.
Article in English | MEDLINE | ID: covidwho-825269
ABSTRACT
Our previous study showed that glycyrrhizin (GLY) inhibited porcine epidemic diarrhea virus (PEDV) infection, but the mechanisms of GLY anti-PEDV action remain unclear. In this study, we focused on the anti-PEDV and anti-proinflammatory cytokine secretion mechanisms of GLY. We found that PEDV infection had no effect on toll-like receptor 4 (TLR4) protein and mRNA levels, but that TLR4 regulated PEDV infection and the mRNA levels of proinflammatory cytokines. In addition, we demonstrated that TLR4 regulated p38 phosphorylation but not extracellular regulated protein kinases1/2 (Erk1/2) and c-Jun N-terminal kinases (JNK) phosphorylation, and that GLY inhibited p38 phosphorylation but not Erk1/2 and JNK phosphorylation. Therefore, we further explored the relationship between high mobility group box-1 (HMGB1) and p38. We demonstrated that inhibition of HMGB1 using an antibody, mutation, or knockdown decreased p38 phosphorylation. Thus, HMGB1 participated in activation of p38 through TLR4. Collectively, our data indicated that GLY inhibited PEDV infection and decreased proinflammatory cytokine secretion via the HMGB1/TLR4-mitogen-activated protein kinase (MAPK) p38 pathway.
Subject(s)
Keywords

Full text: Available Collection: International databases Database: MEDLINE Main subject: Signal Transduction / Glycyrrhizic Acid / HMGB1 Protein / P38 Mitogen-Activated Protein Kinases / Toll-Like Receptor 4 / Porcine epidemic diarrhea virus Limits: Animals Language: English Year: 2020 Document Type: Article Affiliation country: Ijms21082961

Similar

MEDLINE

...
LILACS

LIS


Full text: Available Collection: International databases Database: MEDLINE Main subject: Signal Transduction / Glycyrrhizic Acid / HMGB1 Protein / P38 Mitogen-Activated Protein Kinases / Toll-Like Receptor 4 / Porcine epidemic diarrhea virus Limits: Animals Language: English Year: 2020 Document Type: Article Affiliation country: Ijms21082961