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基于网络药理学的方法鉴定茵黄颗粒治疗代谢相关脂肪性肝病小鼠模型的关键通路。

Network pharmacology-based identification of significant pathway for protection of Yinhuang granule in a mice model of metabolic-associated fatty liver disease.

机构信息

The MOE Key Laboratory for Standardization of Chinese Medicines, Shanghai Key Laboratory of Compound Chinese Medicines and The SATCM Key Laboratory for New Resources and Quality Evaluation of Chinese Medicines, Institute of Chinese Materia Medica, Shanghai University of Traditional Chinese Medicine, 1200 Cailun Road, Shanghai 201203, China.

The MOE Key Laboratory for Standardization of Chinese Medicines, Shanghai Key Laboratory of Compound Chinese Medicines and The SATCM Key Laboratory for New Resources and Quality Evaluation of Chinese Medicines, Institute of Chinese Materia Medica, Shanghai University of Traditional Chinese Medicine, 1200 Cailun Road, Shanghai 201203, China.

出版信息

Phytomedicine. 2021 Oct;91:153666. doi: 10.1016/j.phymed.2021.153666. Epub 2021 Jul 16.

DOI:10.1016/j.phymed.2021.153666
PMID:34339944
Abstract

BACKGROUND

Metabolic-associated fatty liver disease (MAFLD) is a spectrum of liver disorders. Nonalcoholic steatohepatitis (NASH) is defined as a more serious process of MAFLD with liver inflammation.

PURPOSE

This study aims to observe the alleviation of Yinhuang granule (YHG), a Chinese patent medicine, on methionine and choline-deficient diet (MCD)-induced MAFLD in mice.

METHODS

Network pharmacology was used to analyze the improving effect of YHG on MAFLD and possible targets. MAFLD was induced in mice by MCD diet feeding for 6 weeks. In the last 2 weeks, the mice were orally given with YHG (400, 800 mg/kg) every day. Biochemical parameters of serum and liver, as well as hepatic gene expression were detected.

RESULTS

Network pharmacology showed that YHG could improve MAFLD, inflammation, liver fibrosis, and oxidative stress. In animal experiments, YHG reduced hepatocellular damage and hepatic lipids accumulation which induced by MCD. In terms of liver inflammation, YHG attenuated MCD-induced liver inflammation in mice. YHG also inhibited the activation of hepatic stellate cells (HSCs) and alleviated liver fibrosis in MCD-fed mice. Through nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway, YHG alleviated liver oxidative stress injury in mice which induced by MCD.

CONCLUSION

YHG ameliorated MCD-induced MAFLD in mice by reducing hepatic lipids accumulation, alleviating liver oxidative, inflammatory injury and attenuating hepatic fibrosis.

摘要

背景

代谢相关脂肪性肝病(MAFLD)是一系列肝脏疾病。非酒精性脂肪性肝炎(NASH)被定义为 MAFLD 中更严重的肝脏炎症过程。

目的

本研究旨在观察中药茵黄颗粒(YHG)对蛋氨酸胆碱缺乏饮食(MCD)诱导的 MAFLD 小鼠的缓解作用。

方法

采用网络药理学分析 YHG 对 MAFLD 的改善作用及可能靶点。通过 MCD 饮食喂养 6 周诱导 MAFLD 小鼠。在最后 2 周,每天给予 YHG(400、800mg/kg)灌胃。检测血清和肝脏的生化参数以及肝组织基因表达。

结果

网络药理学显示,YHG 可改善 MAFLD、炎症、肝纤维化和氧化应激。在动物实验中,YHG 减轻了 MCD 诱导的肝细胞损伤和肝内脂质蓄积。在肝脏炎症方面,YHG 减轻了 MCD 诱导的小鼠肝炎症。YHG 还通过核因子红细胞 2 相关因子 2(Nrf2)信号通路抑制肝星状细胞(HSCs)的激活,减轻 MCD 喂养小鼠的肝纤维化。通过核因子红细胞 2 相关因子 2(Nrf2)信号通路,YHG 减轻了 MCD 诱导的小鼠肝脏氧化应激损伤。

结论

YHG 通过减少肝内脂质蓄积、减轻肝氧化、炎症损伤和减轻肝纤维化,改善 MCD 诱导的 MAFLD 小鼠。

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