Abstract
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.
Highlights
Antioxidants in food and herbs may prevent free radicalinduced cell damage and inflammatory reactions
We found that 1 μg/ml LPS induced more reactive oxygen species (ROS) compared with the control RAW264.7 cells (Figures 2(a) and 2(b))
We observed that LPS increased MCP-1 expression and decreased the expression of antioxidative stress protein SOD-1
Summary
Antioxidants in food and herbs may prevent free radicalinduced cell damage and inflammatory reactions. Increasing studies have focused on the antioxidative and anti-inflammatory roles [8] of Tremella fuciformis polysaccharides (TFPS). Increasing evidence has indicated that several miRNAs act as key regulators of macrophage activation and inflammatory reaction [12]. Many studies indicated that miR-155 acts as a key mediator of inflammation in atherosclerosis by repressing B-cell and promoting NFκB activation in macrophages [12, 13]. Our results revealed that TFPS could attenuate free radical production and alleviate the inflammatory reaction by regulating the nuclear translocation of NFκB. These findings provide insight into the mechanisms of TFPS in the regulation of macrophage inflammation and a new potential treatment for inflammation-related diseases
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