Purple Sweet Potato Polysaccharide Exerting an Anti-inflammatory Effect via a TLR-Mediated Pathway by Regulating Polarization and Inhibiting the Inflammasome Activation.
J Agric Food Chem
; 72(4): 2165-2177, 2024 Jan 31.
Article
em En
| MEDLINE
| ID: mdl-38233194
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 (Ca2+) 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 Ca2+ 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-ß (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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Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Ipomoea batatas
/
Inflamassomos
Tipo de estudo:
Prognostic_studies
Idioma:
En
Revista:
J Agric Food Chem
Ano de publicação:
2024
Tipo de documento:
Article