In vitro and in vivo studies have shown that chitosan oligosaccharide (COS) has significant anti-inflammatory and antioxidant activities.
In vivo experiments, lipopolysaccharide (LPS) was used to establish a mouse inflammation model. After COS treatment, it was found that COS could not only inhibit organ dysfunction, but also improve the survival rate of inflammatory mice. Numerous experimental studies have shown that COS can inhibit neutrophil infiltration and significantly reduce the levels of circulating proinflammatory factors such as tumor necrosis factor in vivo. (TNF-α), interleukin 1β (IL-1β), etc. Furthermore, catalase enzymes such as glutathione (GSH) and catalase (CAT) were disrupted in mice with LPS-induced inflammation, and COS could reverse this redox imbalance.
Overall, COS can protect mice from LPS by inhibiting inflammatory and oxidative responses. In another study, using a pig model that is closer to humans, the addition of COS to the daily diet significantly attenuated LPS-induced colitis injury, and tumor necrosis factor alpha (TNF-α) in serum and gastrointestinal tract. , Interleukin 6 (IL-6) and interleukin 8 (IL-8) were significantly decreased. The physiological activity of COS in the gastrointestinal tract is mainly related to the MAPK and AMPK signal transduction pathways.
In in vitro experiments, using human umbilical vein endothelial cells (HUVEC) cells as a model, it was found that COS also has anti-inflammatory activity, mainly by inhibiting the over-activation of potassium channels, down-regulating p38 phosphorylation, and promoting the expression of acetoxyglycosyltransferase. expression to inhibit LPS-induced apoptosis. In addition, COS showed inhibitory effect on tumor necrosis factor α (TNF-α) and interleukin 6 (IIL-6) in macrophage RAW264.7.
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