AI Article Synopsis

  • A study investigated the anti-inflammatory effects of a novel glucan derived from purple sweet potatoes, known as PSPP-1, using LPS-induced RAW264.7 cells as an inflammation model.
  • PSPP-1 was found to inhibit cell proliferation and reduce levels of nitric oxide, reactive oxygen species, and calcium ions, while altering the balance of pro-inflammatory and anti-inflammatory cytokines.
  • The research revealed that PSPP-1 triggers anti-inflammatory pathways through TLR2 and TLR4, affects macrophage polarization, and inhibits the activation of the NLRP3 inflammasome, suggesting its potential as a therapeutic agent for inflammatory-related conditions.

Article Abstract

Purple sweet potato polysaccharide (PSPP-1) is a novel glucan; this study aimed to examine the anti-inflammatory effect of PSPP-1 and elucidate its potential mechanisms. Lipopolysaccharide (LPS)-induced RAW264.7 was used as the model of inflammation, cell viability, and levels of nitric oxide (NO), reactive oxygen species (ROS), and calcium ion (Ca) were analyzed. ELISA and qPCR were used to assess the productions and mRNA expression of cytokines, and Western blotting was used to assess protein expressions in the TLR-mediated pathway, macrophage polarization, and inflammasome activation. The results demonstrated PSPP-1 inhibited cell proliferation and markedly decreased NO, ROS, and Ca levels. Moreover, PSPP-1 suppressed the secretions and mRNA expressions of pro-inflammatory cytokines and increased those of anti-inflammatory cytokines. Furthermore, PSPP-1 could exert anti-inflammatory effects through different pathways mediated by both TLR2 and TLR4, which modulated the expressions of essential proteins in the myeloid differentiation factor 88 (MyD88)-dependent and toll/IL-1 receptor domain-containing adaptor-inducing interferon-β (TRIF)-dependent signaling pathways. PSPP-1 even regulated the polarization of M1/M2 macrophages and inhibited the nucleotide oligomerization domain-like receptor protein 3 (NLRP3) inflammasome activation. These findings indicate that PSPP-1 can suppress LPS-induced inflammation via multiple pathways and may be a potential agent for therapeutic inflammation-related pathophysiological processes and disorders.

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Source
http://dx.doi.org/10.1021/acs.jafc.3c07511DOI Listing

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