Inhibitory Effects of Inonotus obliquus Polysaccharide on Inflammatory Response in Toxoplasma gondii-Infected RAW264.7 Macrophages

• Published in: Evidence-based complementary and alternative medicine Vol. 2021; pp. 2245496 - 11
• Main Authors: Yan, Kexin, Zhou, Hongyuan, Wang, Meng, Li, Haitao, Sang, Rui, Ge, Bingjie, Zhao, Xin, Li, Chunting, Wang, Wei, Zhang, Xuemei
• Format: Journal Article
• Language: English
• Published: United States Hindawi 2021; Hindawi Limited
• Subjects: Alzheimer's disease; Antibodies; c-Jun protein; Chemokines; Cytokines; Cytoplasm; Enzyme inhibitors; Extracellular signal-regulated kinase; Gene expression; IL-1β; Infections; Inflammation; Interleukin 4; Interleukin 6; JNK protein; Kinases; Macrophage inflammatory protein; Monocyte chemoattractant protein; Monocyte chemoattractant protein 1; Monocytes; Natural products; NF-κB protein; Phosphorylation; Polysaccharides; Protein kinase; Proteins; Signal transduction; TLR2 protein; TLR4 protein; Toll-like receptors; Toxoplasma gondii; Transcription factors; Tumor necrosis factor-α; γ-Interferon; United States > US; China; Japan
• ISSN: 1741-427X; 1741-4288
• DOI: 10.1155/2021/2245496

Our previous reports have shown that Inonotus obliquus polysaccharide (IOP) has protective effects against Toxoplasma gondii (T. gondii) infection in vivo. The aim of the present research is to explore the in vitro anti-inflammatory effects of IOP and its mechanism in RAW264.7 macrophages infected by T. gondii. In this study, it is indicated that IOP decreased the excessive secretion of inflammatory cytokines tumor necrosis factor-α (TNF-α), interferon-γ (IFN-γ), interleukin-1β (IL-1β), IL-4, and IL-6 in T. gondii-infected RAW264.7 macrophages. IOP effectively suppressed the mRNA expression of these cytokines and chemokines monocyte chemoattractant protein-1 (MCP-1) and macrophage inflammatory protein-1α (MIP-1α). Moreover, IOP inhibited the phosphorylation of inhibitor kappa B kinase α/β (IKKα/β), inhibitor κBα (IκBα), p65 in nuclear factor-kappa B (NF-κB) signaling pathway and p38, c-Jun N-terminal kinase (JNK), and extracellular signal-regulated kinase 1/2 (ERK1/2) in mitogen-activated protein kinases (MAPKs) signaling pathway. Meantime, IOP prevented NF-κB p65 and c-Jun translocation from the cytoplasm to the nucleus. Further, IOP downregulated the protein expression of toll-like receptor 2 (TLR2) and TLR4 in T. gondii-infected RAW264.7 macrophages. The above results suggest that IOP can inhibit the inflammatory response infected with T. gondii via regulating TLR2/TLR4-NF-κB/MAPKs pathways and exerting its anti-T. gondii role in vitro.