Ameliorative Effect of Glycyrrhizic Acid on Diosbulbin B-Induced Liver Injury and Its Mechanism

机制(生物学) 肝损伤 传统医学 药理学 化学 医学 哲学 认识论
作者
Xin Wang,Lubing Shi,Yu-Han Zhang,Hongzhe Zhu,Shan-Shan Cao,Yong Qiang Shi,Huizi Shangguan,Ji-Ping Liu,Yundong Xie
出处
期刊:The American Journal of Chinese Medicine [World Scientific]
卷期号:53 (01): 309-335 被引量:6
标识
DOI:10.1142/s0192415x25500120
摘要

This study aimed to clarify the protective effect of Glycyrrhizic acid (GL) against Diosbulbin B (DB) — induced liver injury in mice and investigate its mechanisms of action. A liver injury DB was established in mice through the oral administration of DB for 15 days. At the same time, GL was administered to the mice for treatment. After the experiment, the pharmacodynamics and mechanisms of GL in ameliorating DB-induced liver injury were explored using biochemical indexes, non-targeted metabolomics, targeted metabolomics, Western blotting analysis of protein expression, 16S rDNA sequencing, and Spearman correlation analysis. The results show reduced liver function indices and improved DB-induced hepatic pathological changes. It also attenuated DB-induced hepatic inflammation and oxidative stress. Hepatic metabolomics revealed that GL regulated ABC transporters and bile secretion. Targeted bile acid (BA) metabolomics and Western blotting demonstrated that GL improved DB-induced reduction in BA efflux by regulating FXR-mediated efflux transporters. Furthermore, analysis of 16S rDNA gene sequencing revealed that GL effectively restored the relative abundance of beneficial bacteria, reduced the relative abundance of harmful bacteria, and reinstated the structure of the intestinal flora. Additionally, correlation analyses between BA and intestinal flora indicated that Firmicutes, Bacteroidota, TDGA, DGA, UDGA, GDGA, THDGA, and HDGA could serve as major markers for DB-induced liver injury. In conclusion, GL significantly improved DB-induced liver injury by increasing the expression of Nrf2/FXR-BSEP/MRP2/P-gp/UGT1A1, promoting BA efflux, regulating intestinal flora, and alleviating inflammation and oxidative stress.
最长约 10秒,即可获得该文献文件

科研通智能强力驱动
Strongly Powered by AbleSci AI
科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
Oo。完成签到,获得积分10
刚刚
刚刚
小蘑菇应助耍酷的友卉采纳,获得10
刚刚
Castiron完成签到,获得积分10
刚刚
慕青应助zxcvbnm采纳,获得10
刚刚
思源应助甜甜友容采纳,获得10
1秒前
渡尘完成签到,获得积分10
1秒前
晓晨完成签到,获得积分10
1秒前
2秒前
科研小白完成签到 ,获得积分10
2秒前
伍声痕完成签到,获得积分10
2秒前
飞快的访蕊完成签到,获得积分20
2秒前
白菜完成签到,获得积分10
3秒前
HRC发布了新的文献求助10
3秒前
渡尘发布了新的文献求助10
3秒前
4秒前
活泼学生完成签到 ,获得积分10
4秒前
愉快的楷瑞完成签到,获得积分10
4秒前
英姑应助不爱喝咖啡采纳,获得10
4秒前
结实的德地完成签到,获得积分10
5秒前
顾安完成签到 ,获得积分10
5秒前
等待的语海完成签到,获得积分10
5秒前
5秒前
Temperature发布了新的文献求助10
5秒前
Angela发布了新的文献求助10
5秒前
舒承旺完成签到,获得积分10
5秒前
虚幻的安白应助阳洋洋采纳,获得30
6秒前
6秒前
nini发布了新的文献求助10
6秒前
6秒前
赘婿应助倾语采纳,获得10
7秒前
molihuakai应助认真笑阳采纳,获得10
7秒前
示羊完成签到,获得积分10
8秒前
爱喝饮料的刺猬完成签到,获得积分10
8秒前
8秒前
goldfish完成签到,获得积分10
8秒前
创创发布了新的文献求助10
8秒前
王思甜完成签到,获得积分20
8秒前
粗犷的小凡完成签到,获得积分10
8秒前
填海完成签到,获得积分10
9秒前
高分求助中
Principles of Economics, 11th Edition 10000
University Physics with Modern Physics, 16th edition 10000
(应助此贴封号)【重要!!请各用户(尤其是新用户)详细阅读】【科研通的精品贴汇总】 10000
Molecular Mechanisms of Photosynthesis, 4th Edition 1000
Organic Reactions, Volume 116 1000
Matrix Methods in Data Mining and Pattern Recognition 510
Social Skills Improvement System-Rating Scales--Chinese Version 500
热门求助领域 (近24小时)
化学 材料科学 医学 生物 纳米技术 工程类 有机化学 化学工程 生物化学 计算机科学 内科学 物理 复合材料 催化作用 细胞生物学 无机化学 光电子学 物理化学 电极 基因
热门帖子
关注 科研通微信公众号,转发送积分 7253566
求助须知:如何正确求助?哪些是违规求助? 8875642
关于积分的说明 18738770
捐赠科研通 6934317
什么是DOI,文献DOI怎么找? 3199947
关于科研通互助平台的介绍 2374675
邀请新用户注册赠送积分活动 2174675