“Unraveling the Neuroprotective Mechanism of Dioscorea bulbifera (DB) in Alzheimer’s Disease (AD) Caused by Estrogen Loss: An Integrated Network Pharmacology Investigation and Experimental Validation”

神经保护 药理学 雌激素 作用机理 去卵巢大鼠 背景(考古学) 神经科学 生物 医学 内分泌学 生物化学 体外 古生物学
作者
Mayank Roy Chowdhury,Anamika Tiwari,Karamveer Karamveer,Govind Prasad Dubey,Basant K. Tiwary,Sudarshana Deepa Vijaykumar
出处
期刊:Alzheimers & Dementia [Wiley]
卷期号:19 (S24)
标识
DOI:10.1002/alz.082817
摘要

Abstract Background Alzheimer’s disease (AD) is a leading cause of dementia, characterized by cognitive decline, and is more prevalent in women, possibly due to estrogen loss after menopause. Dioscorea bulbifera (DB), a medicinal plant, has been proposed as a potential treatment for AD. However, the underlying mechanism of action of DB and its neuroprotective effects in AD, particularly in the context of estrogen loss, remain unclear. Method In this study, we employed an integrative network pharmacology approach to predict the mechanism of action of DB in AD. Using a collection of AD‐related genes and predicted DB targets, we identified putative targets, direct regulatory targets, and potential regulatory targets of DB. Pathway‐enrichment analysis was performed to elucidate the pivotal pathways involved in DB’s treatment of AD. Molecular docking was conducted to verify the interactions between the core targets and the active ingredients of DB. In vivo experiments were conducted using ovariectomized rats induced with scopolamine to evaluate the neuroprotective effects of DB. Acetylcholine (Ach) and serum estradiol levels were quantified using ELISA. Result Our results identified 132 putative targets, including 68 direct regulatory targets and 25 potential regulatory targets of DB for the treatment of AD. Pathway‐enrichment analysis revealed that neurotransmitter clearance in the synaptic cleft was a crucial pathway in the treatment of AD with DB. Molecular docking further supported the interactions between the core targets (ESR1, APP, GSK3β, BACE1, AChE, and MAOB) and the active ingredients of DB. In vivo experiments using ovariectomized rats induced with scopolamine demonstrated the neuroprotective effect of DB and validated the predicted mechanism of action. Conclusion Our findings provide experimental support for the predicted mechanism of action of DB in AD caused by estrogen loss, and validate its neuroprotective effects using behavioral tests and ELISA in ovariectomized rats. DB may hold promise as a potential therapeutic option for AD, particularly in the context of estrogen loss, and further research is warranted to explore its full potential in AD treatment.
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
1秒前
吃饭了发布了新的文献求助10
1秒前
啊啊发布了新的文献求助10
1秒前
3秒前
归途发布了新的文献求助10
3秒前
hhcai完成签到,获得积分10
3秒前
5秒前
酷波er应助科研通管家采纳,获得10
5秒前
澡雪发布了新的文献求助10
5秒前
小二郎应助风趣安青采纳,获得10
5秒前
我是老大应助科研通管家采纳,获得10
5秒前
传奇3应助科研通管家采纳,获得10
5秒前
充电宝应助科研通管家采纳,获得30
5秒前
5秒前
5秒前
上上完成签到,获得积分10
6秒前
1111111111111完成签到,获得积分10
8秒前
9秒前
勤奋静芙完成签到,获得积分20
11秒前
翁雁丝发布了新的文献求助10
12秒前
吃饭了完成签到,获得积分10
12秒前
苗条梦玉发布了新的文献求助10
13秒前
13秒前
14秒前
椰汁味完成签到,获得积分10
15秒前
CC悟了发布了新的文献求助10
17秒前
木子发布了新的文献求助10
17秒前
19秒前
上官若男应助南音采纳,获得10
19秒前
大爷完成签到 ,获得积分10
20秒前
牢大完成签到 ,获得积分10
21秒前
21秒前
领导范儿应助wangxiaobin采纳,获得10
21秒前
852应助翁雁丝采纳,获得10
21秒前
23秒前
徐振阳发布了新的文献求助10
23秒前
Dilmma发布了新的文献求助20
23秒前
May发布了新的文献求助10
26秒前
27秒前
28秒前
高分求助中
A new approach to the extrapolation of accelerated life test data 1000
Picture Books with Same-sex Parented Families: Unintentional Censorship 700
ACSM’s Guidelines for Exercise Testing and Prescription, 12th edition 500
Nucleophilic substitution in azasydnone-modified dinitroanisoles 500
不知道标题是什么 500
Indomethacinのヒトにおける経皮吸収 400
Phylogenetic study of the order Polydesmida (Myriapoda: Diplopoda) 370
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 3975693
求助须知:如何正确求助?哪些是违规求助? 3520019
关于积分的说明 11200635
捐赠科研通 3256410
什么是DOI,文献DOI怎么找? 1798255
邀请新用户注册赠送积分活动 877490
科研通“疑难数据库(出版商)”最低求助积分说明 806390