Nutrients · 2025
Anti-Inflammatory Effect of a Polysaccharide Derived from Artocarpus heterophyllus Lam. Pulp on Lipopolysaccharide-Stimulated RAW264.7 Macrophages Through Inhibiting MAPK/ERK Signaling Pathway.
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Bai Benyan, Liu Mengyang, Xu Panjie, Zhang Yanjun, Xu Fei, Wu Gang, Zhou Yan, Zhu Kexue
Аннотация
BACKGROUND: Inflammation is a critical pathological process implicated in numerous diseases.
METHODS: In this study, a water-soluble polysaccharide was extracted from the fruit pulp of Artocarpus heterophyllus Lam. (namely, JFP-Ps), and the anti-inflammatory properties and underlying mechanisms were investigated. Inflammatory responses were induced in RAW264.7 macrophages through lipopolysaccharide (LPS) stimulation.
RESULTS: JFP-Ps markedly diminished the production of nitric oxide (NO) and reactive oxygen species (ROS); reduced LPS-induced cell apoptosis by increasing glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) activity; and decreased pro-inflammatory cytokine levels, including interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α). JFP-Ps decreased inflammatory responses by inhibiting the production of gene and protein expression associated with the MAPK/ERK pathway. Additionally, metabolomic profiling revealed that LPS stimulation increased ether lipid metabolism while it decreased pantothenate and coenzyme A biosynthesis. These metabolic changes were partially reversed by JFP-Ps through inhibiting the synthesis of branched-chain amino acids.
CONCLUSIONS: JFP-Ps may exert anti-inflammatory effects by concurrently modulating oxidative stress, inflammatory signaling, and metabolic reprogramming in macrophages.
METHODS: In this study, a water-soluble polysaccharide was extracted from the fruit pulp of Artocarpus heterophyllus Lam. (namely, JFP-Ps), and the anti-inflammatory properties and underlying mechanisms were investigated. Inflammatory responses were induced in RAW264.7 macrophages through lipopolysaccharide (LPS) stimulation.
RESULTS: JFP-Ps markedly diminished the production of nitric oxide (NO) and reactive oxygen species (ROS); reduced LPS-induced cell apoptosis by increasing glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) activity; and decreased pro-inflammatory cytokine levels, including interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α). JFP-Ps decreased inflammatory responses by inhibiting the production of gene and protein expression associated with the MAPK/ERK pathway. Additionally, metabolomic profiling revealed that LPS stimulation increased ether lipid metabolism while it decreased pantothenate and coenzyme A biosynthesis. These metabolic changes were partially reversed by JFP-Ps through inhibiting the synthesis of branched-chain amino acids.
CONCLUSIONS: JFP-Ps may exert anti-inflammatory effects by concurrently modulating oxidative stress, inflammatory signaling, and metabolic reprogramming in macrophages.