Division of Gastroenterology and Hepatology, Digestive Disease Institute, Tongji Hospital, Tongji University School of Medicine, Shanghai 200065, China; School of Biomedical Sciences, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong.
Division of Gastroenterology and Hepatology, Digestive Disease Institute, Tongji Hospital, Tongji University School of Medicine, Shanghai 200065, China.
Int J Biol Macromol. 2018 Dec;120(Pt B):1480-1489. doi: 10.1016/j.ijbiomac.2018.09.151. Epub 2018 Sep 25.
Lycium barbarum polysaccharides (LBP) are major bioactive constituents of wolfberry which possess several pharmacological effects such as antioxidant and immunomodulatory activities. We aimed to evaluate how LBP attenuated the hepatic injury in a non-alcoholic steatohepatitis (NASH) methionine-choline deficient (MCD) mouse model. NASH was induced in C57BL/6N mice by feeding with MCD diet for 6 weeks. During the experiments, 1 mg/kg LBP was intragastrically fed on a daily basis with or without MCD diet lasting from the 4th to 6th week. Control and vehicle-control (LBP + PBS) were fed with a regular animal chow. LBP significantly ameliorated NASH-induced injuries, including the increase of serum ALT and AST levels, hepatic oxidative stress, fibrosis, inflammation, and apoptosis. The hepatoprotective effects of LBP were accompanied by the attenuation of thioredoxin interacting protein, nod-like receptor protein 3/6 (NLRP3/6) and reduced NF-κB (nuclear factor-kappa B) activity. Vehicle LBP fed mice showed no adverse effect on the liver. In conclusion, the suppression of the NLRP3/6 inflammasome pathway and NF-κB activation may partly contribute to the reduction of the hepatic injury during the progression of NASH by therapeutic LBP treatment.
枸杞多糖(LBP)是枸杞的主要生物活性成分,具有抗氧化和免疫调节等多种药理作用。我们旨在评估 LBP 如何减轻非酒精性脂肪性肝炎(NASH)蛋氨酸-胆碱缺乏(MCD)小鼠模型中的肝损伤。通过用 MCD 饮食喂养 6 周,在 C57BL/6N 小鼠中诱导 NASH。在实验过程中,从第 4 周到第 6 周,每天通过胃内给予 1mg/kg 的 LBP,无论是否存在 MCD 饮食。对照组和载体对照组(LBP+PBS)用常规动物饲料喂养。LBP 显著改善了 NASH 引起的损伤,包括血清 ALT 和 AST 水平升高、肝氧化应激、纤维化、炎症和细胞凋亡。LBP 的保肝作用伴随着硫氧还蛋白相互作用蛋白、核苷酸结合寡聚化结构域样受体蛋白 3/6(NLRP3/6)和核因子-kappa B(NF-κB)活性的减弱。给予载体 LBP 的小鼠对肝脏没有不良影响。总之,抑制 NLRP3/6 炎性小体途径和 NF-κB 激活可能部分有助于治疗性 LBP 治疗 NASH 进展过程中减轻肝损伤。