Perioperative administration of fucoidan induced changes in immune cell composition and resulted in no beneficiary outcomes in the acute phase of postoperative neurocognitive recovery.

For many of the versatile functions of polysaccharides as natural ingredients in human foods, the immunomodulatory and anti-inflammatory activities of fucoidan, partly owing to its high sulfate content, attracted extensive attention in its potential application in cancer therapy as well as in prevention of neurodegeneration. In this study, we characterized the impact of long-term supplementation of Undaria pinnatifida-derived fucoidan on the gene expression and immune cell abundance in mouse PBMCs. Despite the significantly increased Th17 cells and activated NK cells, naïve B cells were substantially reduced in the PBMCs in fucoidan mice. Fucoidan supplementation induced prominent expression changes in genes associated with Th1/Th2 cell differentiation. Although fucoidan displayed a remarkable anti-inflammatory capacity in our mouse models, perioperative administration of fucoidan failed to show any noticeable beneficiary effect in relieving synaptic and cognitive dysfunction at the acute phase after surgery, which was believed to cause neurocognitive impairment by inducing neuroinflammation. Comparing with that of the mice with control diet, reduced microglia-neuron crosstalk, resulted in compromised neuronal surveillance, was also observed in mice with perioperative administration of fucoidan. In addition, no influence on either basal level or surgery-induced oxidative stress was observed in mice with fucoidan supplementation. Given the complex features of inflammation as the first response to various detrimental situations, we proposed that the anti-inflammation potential of fucoidan, and the changes in immune cell composition induced by which, did not induce favoring changes in mouse brains for impaired cognitive recovery at least at the immediate early postoperative stage.