本研究的目的是评估岩藻黄质（Fx）对脂多糖（LPS）诱导的小鼠肠道屏障损伤的预防作用和潜在机制。我们的结果表明，连续 7 天口服 Fx（每天每公斤体重 50 和 200 毫克）可显着减轻 LPS 诱导的小鼠肠道屏障损伤的严重程度，表现为减轻体重减轻、改善肠道通透性，并改善肠道形态损伤，例如绒毛长度与隐窝深度之比 (V/C) 降低、肠上皮变形、杯状细胞耗竭和粘蛋白 2 (MUC2) 表达低。 Fx 还显着减轻 LPS 诱导的肠上皮细胞 (IEC) 过度凋亡，并抑制回肠和结肠中紧密连接蛋白（包括claudin-1、occludin 和 zonula occlusionns-1）的减少。此外，Fx 还能有效缓解 LPS 诱导的巨噬细胞和中性粒细胞广泛浸润肠粘膜，以及肿瘤坏死因子-α (TNF-α)、白细胞介素 1β (IL-1β) 和 IL-6 等促炎细胞因子的过量产生。和 Gasdermin D (GSDMD) 介导的 IEC 焦亡。其潜在机制可能与抑制核因子κB (NF-κB)、丝裂原激活蛋白激酶(MAPK) 和含有pyrin 结构域的nod 样受体家族3 (NLRP3) 炎症小体信号通路的激活有关。此外，Fx还显着抑制LPS处理小鼠肠道活性氧（ROS）、丙二醛和蛋白质羰基化水平，这可能是通过激活核因子-红细胞2相关因子2（Nrf2）信号通路介导的。总的来说，这些发现表明 Fx 可能被开发为一种潜在的有效膳食补充剂，以预防肠道屏障损伤。

The aim of this study was to evaluate the preventive role and underlying mechanisms of fucoxanthin (Fx) on lipopolysaccharide (LPS)-induced intestinal barrier injury in mice. Our results demonstrated that the oral administration of Fx (50 and 200 mg per kg body weight per day) for consecutive 7 days significantly alleviated the severity of LPS-induced intestinal barrier injury in mice, as evidenced by attenuating body weight loss, improving intestinal permeability, and ameliorating intestinal morphological damage such as reduction in the ratio of the villus length to the crypt depth (V/C), intestinal epithelium distortion, goblet cell depletion, and low mucin 2 (MUC2) expression. Fx also significantly mitigated LPS-induced excessive apoptosis of intestinal epithelial cells (IECs) and curbed the decrease of tight junction proteins including claudin-1, occludin, and zonula occludens-1 in the ileum and colon. Additionally, Fx effectively alleviated LPS-induced extensive infiltration of macrophages and neutrophils into the intestinal mucosa, the overproduction of pro-inflammatory cytokines such as tumor necrosis factor-alpha (TNF-α), interleukin 1beta (IL-1β) and IL-6, and gasdermin D (GSDMD)-mediated pyroptosis of IECs. The underlying mechanisms might be associated with inhibiting the activation of nuclear factor-kappa B (NF-κB), mitogen-activated protein kinases (MAPKs) and nod-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome signaling pathways. Moreover, Fx also notably restrained intestinal reactive oxygen species (ROS), malondialdehyde and protein carbonylation levels in LPS-treated mice, and it might be mediated by activating the nuclear factor-erythroid 2 related factor 2 (Nrf2) signaling pathway. Overall, these findings indicated that Fx might be developed as a potential effective dietary supplement to prevent intestinal barrier injury.