†Natural Product Laboratory, Department of Food Science and Technology, Huazhong Agricultural University, Wuhan, Hubei 430070, People's Republic of China.
§College of Food Science and Engineering, Wuhan Polytechnic University, Wuhan, Hubei 430070, People's Republic of China.
J Agric Food Chem. 2015 Aug 12;63(31):6989-98. doi: 10.1021/acs.jafc.5b01082. Epub 2015 Aug 3.
This study investigated the protective properties of lotus seedpod oligomeric procyanidins (LSOPC) against nonalcoholic fatty liver disease (NAFLD) and its underlying mechanism. Sprague-Dawley (SD) male rats were fed a basic diet, a high-fat diet (HFD), or HFD plus 0.2 or 0.5% (w/w) LSOPC for 12 weeks. Administration of LSOPC markedly reduced serum and hepatic biochemical parameters and protein expression of advanced glycation endproducts (AGEs). Additionally, 0.5% (w/w) LSOPC treatment remarkably reversed the increasing tendency of receptor of advanced glycation endproduct (RAGE) to normal level. Furthermore, dietary LSOPC significantly decreased the protein levels of mitogen-activated protein kinases (MAPK) and nuclear factor-kappa B (NF-κB) and down-regulated genes involved in pro-inflammatory cytokines and adhesion molecules. Taken together, these findings demonstrate that LSOPC may protect obese rats with long-term HFD-induced NAFLD against RAGE-MAPK-NF-κB signaling suppression.
本研究旨在探讨莲子原花青素低聚物（LSOPC）对非酒精性脂肪性肝病（NAFLD）的保护作用及其机制。将 Sprague-Dawley（SD）雄性大鼠分别用基础饲料、高脂饲料（HFD）或 HFD 加 0.2%或 0.5%（w/w）LSOPC 喂养 12 周。LSOPC 的给药显著降低了血清和肝脏生化参数以及晚期糖基化终产物（AGEs）的蛋白表达。此外，0.5%（w/w）LSOPC 处理可显著将受体晚期糖基化终产物（RAGE）的增加趋势恢复到正常水平。此外，膳食 LSOPC 可显著降低丝裂原活化蛋白激酶（MAPK）和核因子-κB（NF-κB）的蛋白水平，并下调与促炎细胞因子和黏附分子相关的基因。综上所述，这些发现表明 LSOPC 可能通过抑制 RAGE-MAPK-NF-κB 信号通路来预防长期 HFD 诱导的肥胖大鼠 NAFLD。
Zotero 插件