Effect Of Ptl On Lps-Induced Macrophage Inflammation Model

This study aims to investigate the immunomodulatory effects of PTL coating on LPS-induced inflammation in RAW264.7 cells in vitro. Through systematic analysis of gene and protein expression levels coupled with phenotypic characterization, this study investigates the molecular mechanisms by which PTL coating mediates immune regulation. An in vitro inflammation model was established using LPS-induced macrophages and subsequently validated. To investigate the effects of PTL coating on macrophage inflammation and activation of the NF-κB-p65 pathway, we assessed gene and protein expression levels, as well as polarization shifts, using qRT-PCR, WB, flow cytometry, and immunofluorescence staining in groups. PTL coating can significantly inhibit the expression of inflammatory cytokines (iNOS, IL-6 and TNF-α) (P<0.05) while promoting the expression of M2-type macrophage markers (CD206, Arg-1 and TGF-β) (P<0.05). In addition, the immunoregulatory effects of PTL coating may be mediated through considerable suppression of NF-κB-p65 protein phosphorylation(P<0.01), inhibition of NF-κB nuclear translocation, and modulation of the M2/M1 macrophage polarization ratio(P<0.001). PTL coating demonstrate a remarkable inhibitory effect on LPS-induced inflammatory responses and M1-type macrophages. It can also greatly suppress NF-κB activation and relative signaling pathways, suggesting that NF-κB may serve as a functional target through which PTL coating exerts its immunomodulatory effects, inhibiting M1-type polarization while promoting M2-type polarization.