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Updated: Feb 9, 2026

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Published on: April 3, 2017
Tremella fuciformis Polysaccharides Attenuate Oxidative Stress and Inflammation in Macrophages through miR-155
Yang Ruan1, Hong Li1, Lianmei Pu1
1Ward Thirty-Three, Department of Emergency Cardiology, Beijing Anzhen Hospital, Capital Medical University, Beijing 100029, China.
Aim:
To investigate the function of Tremella fuciformis polysaccharides (TFPS) in LPS-induced inflammation and oxidative stress of macrophages.
Methods:
RAW264.7 cells were pretreated with TFPS and then stimulated with 0.1 μg/ml LPS. NFκB, Akt, p38MAPK, MCP-1, and SOD-1 were analyzed by Western blotting. Cell viability was measured using MTT assays. Reactive oxygen species (ROS) production, real-time PCR, ELISA, and immunofluorescence staining were performed on RAW264.7 cells that were treated with LPS and/or TFPS to investigate the anti-inflammatory effect of TFPS.
Results:
LPS induced inflammation and ROS production and promoted the secretion of cytokines such as TNF-α and IL-6. LPS also enhanced the nuclear translocation of NFκB, which promoted inflammation by oxidative stress. However, pretreatment with TFPS profoundly inhibited the activation of Akt, p38MAPK, and NFκB and attenuated the expression of MCP-1 in macrophages. Meanwhile, TFPS also decreased cytokine and ROS levels and attenuated cell inflammation after treatment with LPS. Moreover, miR-155, one of the key small RNAs which regulate NFκB and inflammation in macrophages, was significantly downregulated.
Conclusion:
TFPS inhibits LPS-induced oxidative stress and inflammation by inhibiting miR-155 expression and NFκB activation in macrophages, which suggests that TFPS may be a potential reagent for inhibiting the development of inflammation.
Insights
Tremella fuciformis polysaccharides (TFPS) reduce inflammation and oxidative stress in macrophages by inhibiting miR-155 and NFκB activation. TFPS shows potential as an anti-inflammatory agent.
Area of Science:
- Immunology
- Cell Biology
- Pharmacology
Background:
- Lipopolysaccharide (LPS) triggers inflammation and oxidative stress in macrophages.
- Nuclear factor-kappa B (NFκB) signaling pathway is a key regulator of inflammatory responses.
- Oxidative stress and inflammation are implicated in various pathological conditions.
Purpose of the Study:
- To investigate the anti-inflammatory and antioxidant effects of Tremella fuciformis polysaccharides (TFPS) on LPS-induced macrophages.
- To elucidate the underlying molecular mechanisms of TFPS action, focusing on NFκB and miR-155 pathways.
Main Methods:
- RAW264.7 macrophage cell line was used.
- Cells were pretreated with TFPS followed by LPS stimulation.
- Western blotting, MTT assays, ROS measurement, real-time PCR, ELISA, and immunofluorescence were employed.
Main Results:
- LPS induced inflammation, oxidative stress, and elevated cytokine levels (TNF-α, IL-6).
- TFPS pretreatment inhibited LPS-induced activation of Akt, p38MAPK, and NFκB.
- TFPS reduced reactive oxygen species (ROS) production and downregulated miR-155 expression.
Conclusions:
- TFPS exhibits significant anti-inflammatory and antioxidant properties in macrophages.
- TFPS exerts its effects by inhibiting miR-155 expression and NFκB activation.
- TFPS is a potential therapeutic agent for managing inflammatory diseases.
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