Network pharmacology to unveil the mechanism of Moluodan in the treatment of chronic atrophic gastritis

系统药理学 计算生物学 机制(生物学) 细胞生长 细胞 细胞凋亡 炎症 系统生物学 药理学 生物 生物信息学 化学 生物化学 药品 免疫学 哲学 认识论
作者
Wuai Zhou,Huan Zhang,Xin Wang,Jun Kang,WuYan Guo,Lihua Zhou,Huiyun Liu,Menglei Wang,Ruikang Jia,Xinjun Du,Weihua Wang,Bo Zhang,Shao Li
出处
期刊:Phytomedicine [Elsevier BV]
卷期号:95: 153837-153837 被引量:142
标识
DOI:10.1016/j.phymed.2021.153837
摘要

Moluodan (MLD) is a traditional Chinese patent medicine for the treatment of chronic atrophic gastritis (CAG). However, the mechanism of action (MoA) of MLD for treating CAG still remain unclear.Elucidate the MoA of MLD for treating CAG based on network pharmacology.Integrate computational prediction and experimental validation based on network pharmacology.Computationally, compounds of MLD were scanned by LC-MS/MS and the target profiles of compounds were identified based on network-based target prediction method. Compounds in MLD were compared with western drugs used for gastritis by hierarchical clustering of target profile. Key biological functional modules of MLD were analyzed, and herb-biological functional module network was constructed to elucidate combinatorial rules of MLD herbs for CAG. Experimentally, MLD's effect on different biological functional modules were validated from both phenotypic level and molecular level in 1- Methyl-3-nitro-1-nitrosoguanidine (MNNG)-induced GES-1 cells.Computational results show that the target profiles of compounds in MLD can cover most of the biomolecules reported in literature. The MoA of MLD can cover most types of MoA of western drugs for CAG. The treatment of CAG by MLD involved the regulation of various biological functional modules, e.g., inflammation/immune, cell proliferation, cell apoptosis, cell differentiation, digestion and metabolism. Experimental results show that MLD can inhibit cell proliferation, promote cell apoptosis and differentiation, reduce the inflammation level and promote lipid droplet accumulation in MNNG-induced GES-1 cells.The network pharmacology framework integrating computational prediction and experimental validation provides a novel way for exploring the MoA of MLD.
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
更新
PDF的下载单位、IP信息已删除 (2025-6-4)

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
斯文败类应助杜阳辉采纳,获得10
刚刚
1秒前
1秒前
大个应助周游采纳,获得10
1秒前
2秒前
赘婿应助wuy采纳,获得10
2秒前
ffff关注了科研通微信公众号
2秒前
汉堡包应助张瑞宁采纳,获得10
2秒前
2秒前
假发君发布了新的文献求助10
3秒前
猪猪hero发布了新的文献求助10
3秒前
薛定谔的猫完成签到,获得积分10
3秒前
无限师发布了新的文献求助30
4秒前
mysteriousue完成签到,获得积分10
4秒前
4秒前
5秒前
5秒前
strzeng完成签到,获得积分10
6秒前
6秒前
量子星尘发布了新的文献求助10
6秒前
6秒前
幽若宝宝发布了新的文献求助10
7秒前
8秒前
Rondab应助灵巧大地采纳,获得10
8秒前
国际学术交流完成签到,获得积分20
8秒前
肚子没肥发布了新的文献求助10
9秒前
9秒前
9秒前
光能使者发布了新的文献求助10
10秒前
昭荃完成签到 ,获得积分0
10秒前
xiaoyy完成签到,获得积分10
10秒前
开朗艳一发布了新的文献求助10
10秒前
怪咖完成签到,获得积分10
11秒前
朝颜完成签到,获得积分10
11秒前
11秒前
12秒前
天天快乐应助邸泽阳采纳,获得10
12秒前
weijian完成签到,获得积分10
12秒前
qin希望应助小坤同学采纳,获得10
12秒前
恋雅颖月发布了新的文献求助20
13秒前
高分求助中
A new approach to the extrapolation of accelerated life test data 1000
ACSM’s Guidelines for Exercise Testing and Prescription, 12th edition 500
‘Unruly’ Children: Historical Fieldnotes and Learning Morality in a Taiwan Village (New Departures in Anthropology) 400
Indomethacinのヒトにおける経皮吸収 400
Phylogenetic study of the order Polydesmida (Myriapoda: Diplopoda) 370
基于可调谐半导体激光吸收光谱技术泄漏气体检测系统的研究 350
Robot-supported joining of reinforcement textiles with one-sided sewing heads 320
热门求助领域 (近24小时)
化学 材料科学 医学 生物 工程类 有机化学 生物化学 物理 内科学 纳米技术 计算机科学 化学工程 复合材料 遗传学 基因 物理化学 催化作用 冶金 细胞生物学 免疫学
热门帖子
关注 科研通微信公众号,转发送积分 3988827
求助须知:如何正确求助?哪些是违规求助? 3531183
关于积分的说明 11252671
捐赠科研通 3269809
什么是DOI,文献DOI怎么找? 1804780
邀请新用户注册赠送积分活动 881885
科研通“疑难数据库(出版商)”最低求助积分说明 809021