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中国临床药理学与治疗学 ›› 2023, Vol. 28 ›› Issue (3): 241-248.doi: 10.12092/j.issn.1009-2501.2023.03.001

• 基础研究 •    下一篇

水飞蓟宾改善非酒精性脂肪性肝炎小鼠脂质代谢紊乱

蔡祖欢1,邓桃妹1,魏奶杰1,朱丹2,钱斐2,王广基1,张经纬1   

  1. 1中国药科大学药物代谢动力学重点实验室,南京 210009,江苏; 2南京中医药大学附属江苏省中医院,南京 210029,江苏 
  • 收稿日期:2022-04-12 修回日期:2022-05-18 出版日期:2023-03-26 发布日期:2023-04-19
  • 通讯作者: 钱斐,通信作者,男,副主任中医师,讲师,研究方向:肝脏疾病。 E-mail:qianfei198918@163.com 张经纬,共同通信作者,男,研究员,博士生导师,研究方向:药物代谢动力学。 E-mail:zhangjw_cnnj@sina.com
  • 作者简介:蔡祖欢,女,硕士研究生,研究方向:药物代谢动力学。 E-mail:Caihuanhuan3849@outlook.com
  • 基金资助:
    国家自然科学基金面上项目(82173887);江苏省“六大人才高峰”项目(WSN-018)

Silybin ameliorates lipid metabolism disorders in mice with non-alco-holic steatohepatitis

CAI Zuhuan1, DENG Taomei1, WEI Naijie1, ZHU Dan2, QIAN Fei2, WANG Guangji1, ZHANG Jingwei1   

  1. 1Key Laboratory of Drug Metabolism & Pharmacokinetics, China Pharmaceutical University, Nanjing 210009, Jiangsu, China; 2Jiangsu Provincial Hospital of Chinese Medicine, Affiliated to Nanjing University of Chinese Medicine, Nanjing 210029, Jiangsu, China 
  • Received:2022-04-12 Revised:2022-05-18 Online:2023-03-26 Published:2023-04-19

摘要:

目的:研究水飞蓟宾对高脂高胆固醇(high-fat and high-cholesterol, HFHC)饮食诱导的非酒精性脂肪性肝炎(non-alcoholic steatohepati-tis, NASH)小鼠肝脏脂质代谢的调控作用。方法:采用 HFHC饮食喂养小鼠构建 NASH模型,使用生化试剂盒检测血清中甘油三酯(triacylglycer-ol, TAG),总胆固醇(total cholesterol, T-CHO),低密度脂蛋白胆固醇(low-density lipoprotein cho-lesterol, LDL-C)和高密度脂蛋白胆固醇(high-den-sity lipoprotein cholesterol, HDL-C)的水平。H&E染色和油红 O染色用于检测肝组织病理学变化。运用脂质组学检测 NASH小鼠肝脏各类脂质代谢的改变。结果:水飞蓟宾显著抑制 NASH小鼠体重、肝重以及腹部脂肪的增加,降低血清 T-CHO、 TG和 LDL-C的含量,改善肝脏脂滴蓄积和气球样变性,并回调 NASH小鼠肝脏棕榈油酸(C16:1)和多不饱和长链脂肪酸(polyunsaturated long-chain fatty acids, PUFAs)的含量。结论:水飞蓟宾可能通过调节 HFHC饮食诱导的小鼠肝脏脂质代谢异常从而减轻肝脏脂质蓄积和脂毒性。

关键词: 水飞蓟宾, 非酒精性脂肪性肝炎, 脂质代谢

Abstract:

AIM: To investigate the regulatory ef-fects of silybin on hepatic lipid metabolism in mice with non-alcoholic steatohepatitis (NASH) induced by high -fat and high-cholesterol (HFHD) diet. METHODS: Mice were fed a HFHD diet to construct a NASH model, and serum levels of triacylglycerol (TAG), total cholesterol (T-CHO), low-density lipo-protein cholesterol (LDL-C) and high-density lipo-protein cholesterol (HDL-C) were measured using biochemical kits. H&E staining and oil red O stain-ing were used to detect histopathological changes in the liver. Lipidomics was used to detect the alter-ations of hepatic lipid metabolism in NASH mice. 
RESULTS: Silybin significantly inhibited the increase of body weight, liver weight and abdominal fat, de-creased serum T-CHO,TAG and LDL-C levels, im-proved hepatic lipid droplet accumulation and bal-looning degeneration, and back-regulated hepatic palmitoleic acid (C16:1) and polyunsaturated long-chain fatty acids (PUFAs) in NASH mice. CONCLU-SION: Silybin possibly reduced hepatic lipid accu-mulation and lipotoxicity by modulating abnormal hepatic lipid metabolism in mice induced by HFHC diet. 

Key words: silybin, non-alcoholic steatohepatitis, lipid metabolism 

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