林慧萱Hui-Hsuan Lin黃登琪Deng-Chi Huang醫學檢驗暨生物技術學系碩士班2026-10-159999-12-312015https://handle.ncl.edu.tw/11296/7j46vxhttps://scholars.csmu.edu.tw/handle/123456789/22097代謝症候群(metabolic syndrome)為一種包含高血壓(hypertension)、血脂異常(dyslipidemia)、高血糖(hyperglycemia)、肥胖(obesity)等綜合病徵。過去已知蓮蓬(lotus seedpod)具有降血糖、降血壓、降肝火等功能。本研究擬探討蓮蓬水萃物(lotus seedpod extract, LSE)對於代謝症候群之影響，以高脂飲食(high fat diet, HFD)合併鏈脲佐菌素(streptozotocin, STZ)誘發BALB/c小鼠作為代謝症候群模式，再分別以1%和2%之LSE作為試驗組與降血脂藥物simvastatin (30 mg/ml) 作為臨床對照組進行6週餵食後犧牲並分析。在動物實驗中發現，相較於誘導組，LSE試驗組之血糖、血壓以及胰島素阻抗(insulin resistance)皆有明顯改善。在體內發炎反應相關的細胞激素腫瘤壞死因子(tumor necrosis factor-α, TNF-α)和介白素-1 (interleukin-1β, IL-1β)在LSE試驗組亦有下降之趨勢。進一步以切片染色分析肝組織發現LSE能降低油滴空泡及組織纖維化之形成。在抗氧化方面，LSE可促使抗氧化酵素穀胱甘胺酸過氧化酵素(glutathione peroxidase, GPx)和超氧化物岐化酶(superoxide dismutase, SOD)活性增加。最後以西方墨點法(Western blotting)進行分析，LSE能夠抑制發炎反應相關蛋白NF-κB和COX-2之表現、膽固醇生成關鍵酵素HMG CoA reductase及其調控蛋白SREBP-2、以及增加參與在肝醣代謝之調控蛋白Akt與GSK3β磷酸化表現。上述動物實驗結果顯示：LSE具有降血脂、降血糖、抗氧化和抗發炎活性，並能抑制活體中代謝症候群之表徵。另一方面以細胞模式探討LSE其其主要成份epigallocatechin (EGC)對於減少肝臟細胞HepG2脂肪堆積的作用，實驗結果發現LSE或EGC皆可降低油酸(oleic acid, OA)所誘導HepG2細胞內脂肪堆積，並抑制脂質生成及發炎反應相關調控蛋白的表現，此LSE的抑制作用與動物實驗分析得到相同之結果。總結，蓮蓬具有抑制肝臟脂質堆積以及改善代謝症候群之潛力。Metabolic syndrome is characterized by obesity, hypertension, hyperglycemia and dyslipidemia as well as a cluster of risk factors. Along with these risk factors rising, the probability of suffering from cardiovascular disease, diabetes and fatty liver would be increased. In the present study, we aimed to investigate the anti-metabolic syndrome effect of lotus seedpod extract (LSE). First, LSE was demonstrated to be rich in flavonoid, including catechin and epigallocatechin (EGC). In vivo study, the mice were fed high-fat diet (HFD) combined streptozotocin (STZ) supplemented with LSE (1% and 2%) or simvastatin (30 mg/ml), as a clinical control, for 6 weeks. To analyze metabolic syndrome, body weight and epididymal fat accumulation were used as indicators of obesity. Fasting serum glucose, insulin, HOMA-IR, and oral glucose tolerance (OGTT) were used as indicators of insulin resistance. Serum total lipids, including cholesterol, triglyceride (TG), LDL-C, and HDL-C, and blood pressure were also measured. For exploring the possible mechanism for diet-induced metabolic syndrome, adipocytokines (leptin and adiponectin) and proinflammatory factors (TNF-α, IL-1β and IL-6) were measured in serum, as well as the presence of fat droplets and peri-portal fibrosis in liver was examined histologically. Feeding LSE to mice significantly reduced these hallmarks of metabolic syndrome induced by HFD combined STZ treatment. Molecular data showed these influences of LSE might be mediated via SREBP-2/HMG CoA reductase, Akt/GSK3β and NF-κB/COX-2 cascade pathway. LSE improved metabolic syndrome in vivo via possessing hypoglycemic, hypolipidemic, antioxidant and anti-inflammatory activities. Furthermore, we examined the effect of LSE and its main compound on reducing lipid accumulation in hepatic HepG2 cells. The result showed LSE or EGC suppressed oleic acid (OA)-induced lipid accumulation. The expressions of critical molecules involved in cholesterol synthesis and inflammation were attenuated by LSE or ECG in the OA-treated HepG2 cells. These results demonstrate that LSE or EGC inhibits the OA-induced hepatic lipogenesis- and inflammation-related regulatory proteins in vitro. Our data imply that LSE potentially could be developed as an anti-metabolic syndrome agent.代謝症候群蓮蓬肝臟細胞脂質堆積脂質生成發炎反應metabolic syndromelotus seedpodhepatocyteslipid accumulationlipogensisinflammationthesis