Abstract
Acid-hydrolyzed silk peptide (SP) is a valuable material that has been used traditionally to treat various diseases, however, the mechanism by which it affects inflammatory responses is unknown. To examine the effects of SP on inflammatory responses, we used macrophages as a vehicle for examining signaling via toll-like receptor 4 (TLR4), which plays an important role in innate immune responses to pathogenic infections and pathogen-derived molecules such as lipopolysaccharide (LPS). We then confirmed the anti-inflammatory effects of SP by examining lymph node, spleen, and serum samples from C57BL/6 mice injected with LPS. We also used LPS-induced bone marrow-derived macrophages and RAW264.7 cells (a murine macrophage cell line) to identify the mechanism by which SP modulates immune responses via the TLR4 signaling pathway. In addition, we showed that SP prevents LPS-induced production of nitric oxide and reactive oxygen species. In summary, SP inhibits LPS-induced inflammatory responses by modulating the TLR4 signaling pathway.