|Abstract: ||發炎性腸病 (Inflammatory bowel disease, IBD) 在已開發國家是已知的醫療負擔且是發病的重要原因，IBD 的標誌包含克隆氏症 (Crohn's disease) 及潰瘍性結腸炎。骨關節炎 (Osteoarthritis, OA) 是一種關節炎疾病常見的形式，其特徵為關節軟骨退化並造成關節功能障礙。目前已經運用了許多藥理性及非藥理性的策略控制這些疾病，第一種是使用藥物，在短期內似乎有效但通常有一些副作用，包含增加了胃腸道及心血管疾病的風險，且在長期來看效果有限。海藻在藥理學應用中備受關注，是由於其具有許多生物醫學特性，包含抗發炎及抗氧化作用，因此本研究目的為探討麒麟菜萃取物 (Eucheuma cottonii Extract, ECE) 對結腸炎小鼠及肥胖誘導骨關節炎大鼠之改善作用。給予雄性 BALB/c 小鼠 2.5% (w/v) 葡聚糖硫酸鈉 (Dextran sulfate sodium, DSS) 連續七天以誘導結腸炎，使用 ECE 後顯示其可防止體重減輕並降低單位結腸的重量比，ECE 還可降低促炎性細胞因子的表現、增加 IL-10 含量並減輕結腸損傷，因此，富含膳食多醣的 ECE 可以減輕 DSS 誘導的發炎性腸病，因此有望成為治療結腸炎的候選物。使用前十字韌帶橫斷及半月板切除術 (Anterior cruciate ligament transection with partial medial meniscectomy surgery, ACLT+MMx) 誘導肥胖大鼠 OA，且在手術前給予雄性 Sprague-Dawley 大鼠 12周高脂飲食誘導，結果指出ECE 治療五周可降低肥胖大鼠體重、三酸甘油酯、總膽固醇 (Total cholesterol, TC) 及 TC 與高密度脂蛋白膽固醇比例，且 ECE 可下調促炎性細胞因子表現、抑制核因子活化B細胞 κ 輕鏈增強子 (nuclear factor-kappa B, NF-κB) 及細胞外訊號調節激酶 (Extracellular signal regulated kinase, ERK1/2) 表現，造成基質金屬蛋白酶 (Matrix metalloproteinase, MMP)-1 及 MMP-13 含量降低並減弱軟骨降解。這些結果顯示富含膳食多醣的 ECE 可抑制肥胖大鼠 OA 發展，表示其有希望成為治療 OA 之候選物。|
Inflammatory bowel disease (IBD) is a known medical burden in most developed countries and a significant cause of morbidity. The IBD label includes Crohn's disease and ulcerative colitis. Osteoarthritis (OA) is a common form of arthritis diseases, characterized by degeneration of articular cartilage, and leading to joint dysfunction. Some strategies have been used to manage these diseases including pharmacological and non-pharmacological. The first strategy uses drugs and seems effective for a short-time but have some side effects such as increased risk of gastrointestinal and cardiovascular diseases as well as seem not effective for a long time. Seaweeds have received much attention in the pharmacological application due to its various therapeutic properties, including the anti-inflammation and antioxidant effects. Therefore, this study aimed to investigate the ameliorative effects of red seaweed Eucheuma cottonii extract (ECE) in a mice model of colitis and an OA model in obese rat. Colitis was induced in male BALB/c mice by the administration of 2.5% (w/v) dextran sulfate sodium (DSS) for 7 days. After treatment, ECE administration protected against weight loss and decreased the colon weight per length ratio. It also decreased proinflammatory cytokine expressions, increased interleukin (IL)-10 level, and reduced colonic damage. Therefore, a dietary polysaccharide from ECE suppressed DSS-induced bowel inflammation, thereby becoming a promising candidate for the treatment of colitis. For OA model, an anterior cruciate ligament transection with partial medial meniscectomy surgery (ACLT+MMx) to induce osteoarthritis characteristics in obese rats. The male Sprague-Dawley rats were fed a high-fat diet for 12 weeks before the surgery. Treatment with ECE for 5 weeks decreased the body weight, triglyceride, and total cholesterol (TC) levels, and the TC/high-density lipoprotein-cholesterol ratio in obese rats. ECE also downregulated the expression of proinflammatory cytokines, suppressed nuclear factor-kappa B and extracellular-signal-regulated kinase-1/2 expressions, resulting in decreased levels of matrix metalloproteinase (MMP)-1 and MMP-13 and attenuated cartilage degradation. These results demonstrated that the dietary polysaccharide from ECE suppressed OA development in obese rats, suggesting its potential efficacy against OA.