Dietary Silk Peptide Inhibits LPS-Induced Inflammatory Responses by Modulating Toll-Like Receptor 4 (TLR4) Signaling

Sungwoo Chei1, Hyun-Ji Oh1, Kippeum Lee1

  • 1Department of Biomedical Sciences, CHA University, Gyeonggi-do 13488, Korea.

Biomolecules
|May 21, 2020
PubMed

Insights

Acid-hydrolyzed silk peptide (SP) inhibits inflammation by modulating the toll-like receptor 4 (TLR4) signaling pathway. This study investigated SP

Area of Science:

  • Immunology
  • Biochemistry
  • Materials Science

Background:

  • Acid-hydrolyzed silk peptide (SP) has traditional uses in medicine, but its anti-inflammatory mechanisms are unclear.
  • Toll-like receptor 4 (TLR4) is crucial for innate immunity, responding to pathogens and molecules like lipopolysaccharide (LPS).

Purpose of the Study:

  • To elucidate the mechanism by which silk peptide (SP) modulates inflammatory responses.
  • To investigate the role of SP in regulating the toll-like receptor 4 (TLR4) signaling pathway.

Main Methods:

  • Utilized macrophages (RAW264.7 cells and bone marrow-derived macrophages) to study TLR4 signaling.
  • Administered LPS to C57BL/6 mice and analyzed lymph node, spleen, and serum samples.
  • Assessed nitric oxide and reactive oxygen species production in LPS-induced cellular models.

Main Results:

  • Silk peptide (SP) demonstrated anti-inflammatory effects in vivo, as evidenced by analysis of mouse tissues and serum.
  • SP was shown to inhibit LPS-induced nitric oxide and reactive oxygen species production in macrophage cell lines.
  • SP modulates immune responses through the TLR4 signaling pathway.

Conclusions:

  • Acid-hydrolyzed silk peptide (SP) effectively inhibits lipopolysaccharide (LPS)-induced inflammatory responses.
  • The anti-inflammatory action of SP is mediated by the modulation of the TLR4 signaling pathway.

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