Abstract
Many studies have reported the biological activities of retrofractamide C (RAC). However, few studies have investigated the anti-inflammatory effect of RAC. In the present study, we investigated the anti-inflammatory effect of RAC using lipopolysaccharide (LPS)-induced J774A.1 cells and a xylene-induced mouse ear edema model. Treatment with RAC decreased LPS-induced nitric oxide (NO) and prostaglandin E2 (PGE2) secretion and inducible NO synthase (iNOS) and cyclooxygenase 2 (COX2) protein expression. It also downregulated the LPS-induced production of interleukin-1β (IL-1β) and interleukin-6 (IL-6) but not tumor necrosis factor α (TNF-α). In the LPS-induced signaling pathway, RAC inhibited the phosphorylation of extracellular signal-regulated kinase (ERK) and nuclear factor kappa light chain enhancer of activated B cells (NF-κB) but not c-Jun N-terminal kinase (JNK) or p38. In a xylene-induced mouse ear edema model, RAC treatment alleviated edema formation and inflammatory cell infiltration. In conclusion, the present study indicates that RAC has the potential to have anti-inflammatory effects and could be a prospective functional food.
Highlights
The role of the inflammatory response is to defend the body against infection and tissue injury [1,2,3].The inflammatory response is initiated by recognition of pathogen-associated molecular patterns (PAMPs) of foreign substances or damage-associated molecular patterns (DAMPs) of injured tissue by pattern recognition receptors (PRRs) of residing or circulating immune cells, such as macrophages, mast cells, fibroblasts and leukocytes [3,4]
nitric oxide (NO) and prostaglandin E2 (PGE2) are major mediators of the inflammatory response. Their biosynthesis is significantly upregulated in inflamed regions, and they contribute to the pathogenesis of inflammatory disorders [30,31]
PGE2 synthesis is initiated with arachidonic acid formation from phospholipids of the cell membrane by phospholipase A2 (PLA2)
Summary
The inflammatory response is initiated by recognition of pathogen-associated molecular patterns (PAMPs) of foreign substances or damage-associated molecular patterns (DAMPs) of injured tissue by pattern recognition receptors (PRRs) of residing or circulating immune cells, such as macrophages, mast cells, fibroblasts and leukocytes [3,4]. Once a PRR binds its agonist, downstream signaling pathways, including mitogen-activated protein kinases (MAPKs) and the nuclear factor kappa light chain enhancer. (AP-1), which is activated by MAPKs, and NF-κB upregulate proinflammatory gene expression [5,6,7,8]. The inflammatory response is mediated and maintained by upregulated proinflammatory cytokines and chemokines. The response induces immune cells to remove pathogenic factors but is often accompanied by pain, vasodilation and fever [9,10]. Acute and chronic inflammatory responses can cause inflammatory diseases, such as sepsis, ulcerative colitis, rheumatoid arthritis and asthma [11,12,13,14]
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