1.研究結果：
Pretreatment with fucoxanthin inhibited histopathological changes in lung tissues and neutrophil infiltration into bronchoalveolar lavage fluid induced by LPS in ALI mice. Moreover, LPS-induced proinflammatory cytokine expression and neutrophil infiltration were inhibited by fucoxanthin in a concentration-dependent manner. Pretreatment of mice with fucoxanthin inhibited NF-κB phosphorylation and IκB degradation in the lungs of mice with LPS-induced ALI. We further found that phosphorylation of Akt and p38 mitogen-activated protein KINASE (MAPK) was inhibited by fucoxanthin. By contrast, the phosphorylation of extracellular signal-regulated kinase and c-Jun N-terminal kinase was not inhibited by fucoxanthin. Furthermore, we found that the activation of RhoA was inhibited by fucoxanthin in LPS-induced ALI.
2.研究貢獻與臨床應用：
On the basis of these results, we propose that fucoxanthin disrupts the RhoA activation-mediated phosphorylation of Akt and p38 MAPK, leading to NF-κB activation in mice with LPS-induced ALI.
基於這些結果，我們建議岩藻黃質破壞 RhoA 激活介導的 Akt 和 p38 MAPK 磷酸化，導致 LPS 誘導的 ALI 小鼠的 NF-κB 激活。期望藉由開發岩藻黃質產品成為緩解急性發炎性肺病發生的藥品，以達到降低急性發炎肺病症狀與死亡率為目標。
