Inhibitory effects of oligochitosan on TNF-α, IL-1β and nitric oxide production in lipopolysaccharide-induced RAW264.7 cells
Jie Zhu, Yuanyuan Zhang, Guoyou Wu, Zhen Xiao, Huanqin Zhou, Xiaomei Yu
Abstract
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Jie Zhu, Yuanyuan Zhang, Guoyou Wu, Zhen Xiao, Huanqin Zhou, Xiaomei Yu
Abstract
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Oligochitosan has been reported to possess anti-inflammatory properties; however, the mechanism of the antiinflammatory effects of oligochitosan remains unknown. The present study aimed to investigate the expression levels of inflammatory cytokines and the production of nitric oxide (NO), in the nuclear factor (NF)-κB pathway of lipopolysaccharide (LPS)-stimulated RAW264.7 murine macrophages. The results of the present study demonstrated that different concentrations of oligochitosan could significantly lower the levels of NO, tumor necrosis factor (TNF)-α and interleukin (IL)-1β, released from LPS-stimulated RAW264.7 cells. This was shown to be mediated through inhibiting the activation of the NF-κB pathway. These results demonstrate that oligochitosan may efficiently inhibit inflammation and has the potential to be an effective anti-inflammatory agent.
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Oligochitosan has been reported to possess anti-inflammatory properties; however, the mechanism of the antiinflammatory effects of oligochitosan remains unknown. The present study aimed to investigate the expression levels of inflammatory cytokines and the production of nitric oxide (NO), in the nuclear factor (NF)-κB pathway of lipopolysaccharide (LPS)-stimulated RAW264.7 murine macrophages. The results of the present study demonstrated that different concentrations of oligochitosan could significantly lower the levels of NO, tumor necrosis factor (TNF)-α and interleukin (IL)-1β, released from LPS-stimulated RAW264.7 cells. This was shown to be mediated through inhibiting the activation of the NF-κB pathway. These results demonstrate that oligochitosan may efficiently inhibit inflammation and has the potential to be an effective anti-inflammatory agent.
Key concepts: Nitric oxide, Lipopolysaccharide, Tumor necrosis factor alpha, Inflammation, Oncogene, Apoptosis, NF-κB, Interleukin