Novel biphasic role of resolvin D1 on expression of cyclooxygenase-2 in lipopolysaccharide-stimulated lung fibroblasts is partly through PI3K/AKT and ERK2 pathways

Research output: Contribution to journalArticle


  • Derong Wu
  • Shengxing Zheng
  • Wenjuan Li
  • Li Yang
  • Yongjian Liu
  • Xia Zheng
  • Yi Yang
  • Liangmin Yang
  • Qian Wang
  • Shengwei Jin

Colleges, School and Institutes


Fibroblasts, far from being merely bystander cells, are known to play a specific role in inflammation resolution after an acute injury. As the endogenous "braking signal," resolvins possess potent anti-inflammatory and pro-resolution actions. We demonstrated that the expression of COX-2 protein was significantly peaked initially at 6 hours but then also at 48 hours after LPS stimulation in lung fibroblasts. PGE2 levels also peaked at 6 hours, and PGD2 levels were increased and peaked at 48 hours. However, no significant change in the protein expression of COX-1 was observed after treatment with LPS in lung fibroblasts. Exogenous resolvin D1 inhibited the first peak of COX-2 expression as well as the production of PGE2 induced by LPS. In contrast, exogenous resolvin D1 increased the second peak of COX-2 expression as well as the production of PGD2 induced by LPS. In addition, resolvin D1 inhibited COX-2 expression at 6 hours, which was partly through PI3K/AKT and ERK2 signalling pathways.


Original languageEnglish
Pages (from-to)964012
JournalMediators of Inflammation
Publication statusPublished - 2013


  • Animals, Cell Line, Chemokine CCL2, Cyclooxygenase 2, Dinoprostone, Docosahexaenoic Acids, Fibroblasts, Gene Expression Regulation, Humans, Interleukin-8, Lipopolysaccharides, Lung, MAP Kinase Signaling System, Mitogen-Activated Protein Kinase 1, Phosphatidylinositol 3-Kinases, Prostaglandin D2, Proto-Oncogene Proteins c-akt, Rats, Signal Transduction