Liu Zhongliang, Ye Jiena, Xi Jiachen, Li Qingping, Tang Yunping, Tian Yizhou, Wang Dongxu, Yang Zuisu, Ding Yaping
Zhoushan Hospital of Traditional Chinese Medicine Affiliated to Zhejiang Chinese Medical University Zhoushan China.
School of Food and Pharmacy Zhejiang Ocean University Zhoushan China.
Food Sci Nutr. 2025 Jul 10;13(7):e70589. doi: 10.1002/fsn3.70589. eCollection 2025 Jul.
Liver fibrosis, closely linked to oxidative stress, remains a significant global health challenge. Fucoxanthin (Fx), a marine carotenoid extracted from brown algae, exhibits potent antioxidant properties, yet its molecular mechanism in liver fibrosis remains unclear. In the present study, a murine model of liver fibrosis was established through intraperitoneal injection of carbon tetrachloride (CCl) to investigate the therapeutic potential and underlying mechanisms of Fx. Histological staining and transmission electron microscopy were utilized to evaluate liver morphology, while assessments were conducted on hepatic function indicators, antioxidant indices, liver fibrosis markers, and inflammatory factors. Notably, treatment with Fx resulted in a significant improvement in serum liver function indicators compared to CCl model mice. Furthermore, the levels of liver fibrosis markers and inflammatory factors were significantly decreased following Fx treatment. Moreover, Fx treatment led to a significant downregulation of hydroxyproline and alpha-smooth muscle actin (α-SMA) expression, while upregulating key antioxidative and ferroptosis-related proteins. These proteins include nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), NAD(P)H:quinone oxidoreductase 1 (NQO1), glutamate-cysteine ligase modifier (GCLM), glutathione peroxidase 4 (GPX4), solute carrier family 7 member 11 (SLC7A11), transferrin receptor 1 (TFR1), and ferritin light chain (FTL) protein expression, in comparison to the CCl model mice. These findings suggest that Fx could effectively ameliorate liver fibrosis by mitigating CCl-induced oxidative stress and ferroptosis, highlighting its therapeutic potential in liver fibrosis management.
肝纤维化与氧化应激密切相关，仍然是一项重大的全球健康挑战。岩藻黄质（Fx）是一种从褐藻中提取的海洋类胡萝卜素，具有强大的抗氧化特性，但其在肝纤维化中的分子机制仍不清楚。在本研究中，通过腹腔注射四氯化碳（CCl）建立了肝纤维化小鼠模型，以研究Fx的治疗潜力和潜在机制。利用组织学染色和透射电子显微镜评估肝脏形态，同时对肝功能指标、抗氧化指标、肝纤维化标志物和炎症因子进行评估。值得注意的是，与CCl模型小鼠相比，Fx治疗使血清肝功能指标有显著改善。此外，Fx治疗后肝纤维化标志物和炎症因子水平显著降低。此外，Fx治疗导致羟脯氨酸和α-平滑肌肌动蛋白（α-SMA）表达显著下调，同时上调关键的抗氧化和铁死亡相关蛋白。与CCl模型小鼠相比，这些蛋白包括核因子红细胞2相关因子2（Nrf2）、血红素加氧酶-1（HO-1）、NAD（P）H：醌氧化还原酶1（NQO1）、谷氨酸-半胱氨酸连接酶修饰剂（GCLM）、谷胱甘肽过氧化物酶4（GPX4）、溶质载体家族7成员11（SLC7A11）、转铁蛋白受体1（TFR1）和铁蛋白轻链（FTL）蛋白表达。这些发现表明，Fx可以通过减轻CCl诱导的氧化应激和铁死亡来有效改善肝纤维化，突出了其在肝纤维化管理中的治疗潜力。
