Background: There are few studies on the autophagy and inflammatory effects of soy peptides on the inflammatory cell model. Further insight into the underlying relationship of soybean peptides and autophagy needs to be addressed. Therefore, it is worthwhile investigating the possible mechanisms of soybean peptides, especially autophagy and the inflammatory effects.
Objective: In this study, we used a RAW264.7 cell inflammation model to study the inhibitory effect and mechanism of soybean peptide QRPR on inflammation.
Methods: We used LPS-induced inflammation model in RAW264.7 cells to study the inhibitory effect and mechanism of soybean peptide QRPR on inflammation. First, Cell viability was determined by cell activity assay. Subsequently, the concentrations of the inflammatory cytokines IL-6 and TNF-α were measured by ELISA. IL-6, TNF-α, Beclin1, LC3, P62, PIK3, AKT, p-AKT, pmTOR and mTOR protein expression were detected by western-blot. PIK3, AKT and mTOR gene expression level were quantified by quantitative real-time PCR. Double-membrane structures of autophagosomes and autolysosomes were observed by transmission electron microscopy. The PI3K/AKT/mTOR signaling pathway in LPS-induced RAW264.7 cells was speculated when the autophagy was activated.
Results: The results showed that QRPR activates autophagy in the inflammatory cell model and that the inhibitory effect of QRPR on inflammation is reduced after autophagy was inhibited. Western- blot and real-time PCR results indicated that QRPR activates autophagy in LPS-induced RAW264.7 cells by modulating the PI3K/AKT/mTOR signaling pathway, and it shows a significant time dependence.
Conclusion: This study indicated that the soybean peptide QRPR activates autophagy and attenuates the inflammatory response in the LPS-induced RAW264.7 cell model.
Keywords: IL-6; PI3K/AKT/mTOR; RAW264.7 cells; TNF-α; autophagy; inflammation; soybean peptides..
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