To investigate the hepatoprotective activities of a polysaccharide extracted from the fruit of Ribes odoratum Wendl. (ROWFP) in a mouse model of high-fat-sucrose diet (HFD)-induced nonalcoholic fatty liver disease (NAFLD). The NAFLD model was induced in C57BL/6 mice by feeding them an HFD for 12 weeks. The mice were randomly divided into the following 5 groups: control group, HFD group, 10-mg/kg ROWFP group, 100-mg/kg ROWFP group, and 200-mg/kg ROWFP group. The levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), total triglycerides (TG), total cholesterol (TC), and high-density lipoprotein (HDL) in the serum were analyzed by enzyme-linked immunosorbent assay. The liver ultrastructure was observed via optical microscopy. The oil red O-stained lipid droplets of the fresh liver samples were analyzed, and the lipid content was semiquantified. CD68 expression in the liver tissue and serum levels of the inflammatory factors (interleukin [IL]-1β, IL-6, and tumor necrosis factor-alpha [TNF-α]) were measured to reflect the inflammation status. The degree of liver fibrosis was determined by sirius red staining. When compared with the control group, the levels of AST, ALT, TG, TC, IL-1β, IL-6, TNF-α, and CD68 in the HFD group were increased, while the HDL level was decreased. Severe liver damage, lipid accumulation, and liver fibrosis were also observed in the HFD model group. When compared with the model group, ROWFP treatment (100 mg/kg or 200 mg/kg) significantly attenuated the HFD-induced hepatic damage. This study supports the hepatoprotective effect of ROWFP against HFD-induced NAFLD.

为了研究从果实中提取的多糖的保肝活动糖茶玉竹温德尔 （ROWFP）在高脂蔗糖饮食（HFD）诱导的非酒精性脂肪肝疾病（NAFLD）的小鼠模型中。通过喂食HFD 12周，在C57BL / 6小鼠中诱导出NAFLD模型。将小鼠随机分为以下5组：对照组，HFD组，10mg / kg ROWFP组，100mg / kg ROWFP组和200mg / kg ROWFP组。用酶联免疫吸附法分析血清中丙氨酸转氨酶（ALT），天冬氨酸转氨酶（AST），总甘油三酯（TG），总胆固醇（TC）和高密度脂蛋白（HDL）的水平。通过光学显微镜观察肝脏的超微结构。分析新鲜肝脏样品的油红色O染色脂质滴，并对脂质含量进行半定量。测量肝脏组织中CD68的表达和血清炎症因子（白介素[IL]-1β，IL-6和肿瘤坏死因子-α[TNF-α]）的水平，以反映炎症状态。肝纤维化程度通过天狼星红染色确定。与对照组相比，HFD组的AST，ALT，TG，TC，IL-1β，IL-6，TNF-α和CD68的水平升高，而HDL的水平降低。在HFD模型组中也观察到严重的肝损伤，脂质蓄积和肝纤维化。与模型组相比，ROWFP治疗（100 mg / kg或200 mg / kg）显着减轻了HFD诱导的肝损伤。这项研究支持ROWFP对HFD诱导的NAFLD的肝保护作用。测量肿瘤坏死因子-α（TNF-α）和TNF-α以反映炎症状态。肝纤维化程度通过天狼星红染色确定。与对照组相比，HFD组的AST，ALT，TG，TC，IL-1β，IL-6，TNF-α和CD68的水平升高，而HDL的水平降低。在HFD模型组中也观察到严重的肝损伤，脂质蓄积和肝纤维化。与模型组相比，ROWFP治疗（100 mg / kg或200 mg / kg）显着减轻了HFD诱导的肝损伤。这项研究支持ROWFP对HFD诱导的NAFLD的肝保护作用。测量肿瘤坏死因子-α（TNF-α）和TNF-α以反映炎症状态。肝纤维化程度通过天狼星红染色确定。与对照组相比，HFD组的AST，ALT，TG，TC，IL-1β，IL-6，TNF-α和CD68的水平升高，而HDL的水平降低。在HFD模型组中也观察到严重的肝损伤，脂质蓄积和肝纤维化。与模型组相比，ROWFP治疗（100 mg / kg或200 mg / kg）显着减轻了HFD诱导的肝损伤。该研究支持ROWFP对HFD诱导的NAFLD的肝保护作用。高密度脂蛋白水平降低。在HFD模型组中也观察到严重的肝损伤，脂质蓄积和肝纤维化。与模型组相比，ROWFP治疗（100 mg / kg或200 mg / kg）显着减轻了HFD诱导的肝损伤。这项研究支持ROWFP对HFD诱导的NAFLD的肝保护作用。高密度脂蛋白水平降低。在HFD模型组中也观察到严重的肝损伤，脂质蓄积和肝纤维化。与模型组相比，ROWFP治疗（100 mg / kg或200 mg / kg）显着减轻了HFD诱导的肝损伤。这项研究支持ROWFP对HFD诱导的NAFLD的肝保护作用。