Tsai Ming-Yang, Yang Wei-Cheng, Lin Chuen-Fu, Wang Chao-Min, Liu Hsien-Yueh, Lin Chen-Si, Lin Jen-Wei, Lin Wei-Li, Lin Tzu-Chun, Fan Pei-Shan, Hung Kuo-Hsiang, Lu Yu-Wen, Chang Geng-Ruei
Animal Industry Division, Livestock Research Institute, Council of Agriculture, Executive Yuan, 112 Muchang, Xinhua Dist, Tainan 71246, Taiwan.
Graduate Institute of Bioresources, National Pingtung University of Science and Technology, 1 Shuefu Road, Neipu, Pingtung 91201, Taiwan.
Molecules. 2021 Mar 30;26(7):1937. doi: 10.3390/molecules26071937.
Liver disorders have been recognized as one major health concern. Fucoidan, a sulfated polysaccharide extracted from the brown seaweed Fucus serratus, has previously been reported as an anti-inflammatory and antioxidant. However, the discovery and validation of its hepatoprotective properties and elucidation of its mechanisms of action are still unknown. The objective of the current study was to investigate the effect and possible modes of action of a treatment of fucoidan against thioacetamide (TAA)-induced liver injury in male C57BL/6 mice by serum biochemical and histological analyses. The mouse model for liver damage was developed by the administration of TAA thrice a week for six weeks. The mice with TAA-induced liver injury were orally administered fucoidan once a day for 42 days. The treated mice showed significantly higher body weights; food intakes; hepatic antioxidative enzymes (catalase, glutathione peroxidase (GPx), and superoxide dismutase (SOD)); and a lower serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and C-reactive protein (CRP) levels. Additionally, a reduced hepatic IL-6 level and a decreased expression of inflammatory-related genes, such as cyclooxygenase-2 (COX-2), and inducible nitric oxide synthase (iNOS) mRNA was observed. These results demonstrated that fucoidan had a hepatoprotective effect on liver injury through the suppression of the inflammatory responses and acting as an antioxidant. In addition, here, we validated the use of fucoidan against liver disorders with supporting molecular data.
肝脏疾病已被公认为一个主要的健康问题。岩藻依聚糖是一种从锯齿墨角藻这种褐藻中提取的硫酸化多糖,此前已有报道称其具有抗炎和抗氧化作用。然而,其肝脏保护特性的发现与验证以及作用机制的阐明仍不明确。本研究的目的是通过血清生化和组织学分析,研究岩藻依聚糖治疗对雄性C57BL/6小鼠硫代乙酰胺(TAA)诱导的肝损伤的影响及可能的作用方式。通过每周三次给予TAA,持续六周来建立肝损伤小鼠模型。对TAA诱导肝损伤的小鼠每天口服岩藻依聚糖,持续42天。接受治疗的小鼠体重、食物摄入量、肝脏抗氧化酶(过氧化氢酶、谷胱甘肽过氧化物酶(GPx)和超氧化物歧化酶(SOD))显著更高;血清丙氨酸氨基转移酶(ALT)、天冬氨酸氨基转移酶(AST)、肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)和C反应蛋白(CRP)水平更低。此外,观察到肝脏IL-6水平降低以及炎症相关基因如环氧化酶-2(COX-2)和诱导型一氧化氮合酶(iNOS)mRNA的表达减少。这些结果表明,岩藻依聚糖通过抑制炎症反应和作为抗氧化剂对肝损伤具有肝脏保护作用。此外,在此我们用支持性的分子数据验证了岩藻依聚糖对肝脏疾病的治疗作用。