Evidence map›Paper›PMID 38676511›Full record

ArticleCombinatorial chemistry & high throughput screening2025

The NeuroProtect Formula: A Preventive Approach to AD Targeting the HIF-1/PI3K-AKT Signaling Pathway Evaluated through

Haiyan Li, Qian Hua, Shuo Cheng, Xiaoge Liu, Qingyuan Cai, Jiani Zhang, Tiantian Peng, Jiao Li, Chunxiang Wang, Chengbang Liang and 3 more

Abstract read
PubMed Publisher
In one paragraph

Article in Combinatorial chemistry & high throughput screening, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.3field-weighted citation impact, top 42% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed, 1 citations in OpenAlex.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors at 1 institution in 1 country.

Haiyan LiSchool of Life Sciences, School of Traditional Chinese Medicine, School of Acupuncture-Moxibustion and Tuina, Beijing University of Chinese Medicine, No. 11 North 3rd Ring, Eastern Road, Beijing, 100029, China.ORCID 0000-0002-1929-8666
Qian HuaSchool of Life Sciences, School of Traditional Chinese Medicine, School of Acupuncture-Moxibustion and Tuina, Beijing University of Chinese Medicine, No. 11 North 3rd Ring, Eastern Road, Beijing, 100029, China.
Shuo ChengSchool of Life Sciences, School of Traditional Chinese Medicine, School of Acupuncture-Moxibustion and Tuina, Beijing University of Chinese Medicine, No. 11 North 3rd Ring, Eastern Road, Beijing, 100029, China.
Xiaoge LiuSchool of Life Sciences, School of Traditional Chinese Medicine, School of Acupuncture-Moxibustion and Tuina, Beijing University of Chinese Medicine, No. 11 North 3rd Ring, Eastern Road, Beijing, 100029, China.
Qingyuan CaiSchool of Life Sciences, School of Traditional Chinese Medicine, School of Acupuncture-Moxibustion and Tuina, Beijing University of Chinese Medicine, No. 11 North 3rd Ring, Eastern Road, Beijing, 100029, China.
Jiani ZhangSchool of Life Sciences, School of Traditional Chinese Medicine, School of Acupuncture-Moxibustion and Tuina, Beijing University of Chinese Medicine, No. 11 North 3rd Ring, Eastern Road, Beijing, 100029, China.
Tiantian PengSchool of Life Sciences, School of Traditional Chinese Medicine, School of Acupuncture-Moxibustion and Tuina, Beijing University of Chinese Medicine, No. 11 North 3rd Ring, Eastern Road, Beijing, 100029, China.
Jiao LiSchool of Life Sciences, School of Traditional Chinese Medicine, School of Acupuncture-Moxibustion and Tuina, Beijing University of Chinese Medicine, No. 11 North 3rd Ring, Eastern Road, Beijing, 100029, China.
Chunxiang WangSchool of Life Sciences, School of Traditional Chinese Medicine, School of Acupuncture-Moxibustion and Tuina, Beijing University of Chinese Medicine, No. 11 North 3rd Ring, Eastern Road, Beijing, 100029, China.
Chengbang LiangSchool of Life Sciences, School of Traditional Chinese Medicine, School of Acupuncture-Moxibustion and Tuina, Beijing University of Chinese Medicine, No. 11 North 3rd Ring, Eastern Road, Beijing, 100029, China.
Yu ShiSchool of Life Sciences, School of Traditional Chinese Medicine, School of Acupuncture-Moxibustion and Tuina, Beijing University of Chinese Medicine, No. 11 North 3rd Ring, Eastern Road, Beijing, 100029, China.
Xu WangSchool of Life Sciences, School of Traditional Chinese Medicine, School of Acupuncture-Moxibustion and Tuina, Beijing University of Chinese Medicine, No. 11 North 3rd Ring, Eastern Road, Beijing, 100029, China.
Yan TanSchool of Life Sciences, School of Traditional Chinese Medicine, School of Acupuncture-Moxibustion and Tuina, Beijing University of Chinese Medicine, No. 11 North 3rd Ring, Eastern Road, Beijing, 100029, China.
Beijing University of Chinese Medicine · CN

Funding

National Natural Science Foundation of China U21A201401, 82374175
6 · The paper itself

Abstract

objectiveAlzheimer's Disease (AD) is a progressive neurodegenerative disorder with limited options for reversing its middle-to-late stages. Early intervention is crucial to slow down disease progression. This study aimed to investigate the potential of the NeuroProtect (NP) formula, a combination of geniposide and Panax notoginseng saponins, in preventing AD. We evaluated the effects of the NP formula on amyloid plaque accumulation, neuronal degeneration, and molecular signaling pathways using

methodsTo predict functional pathways and potential downstream targets of NP intervention, we employed network pharmacology. The preventative impact of the NP formula was assessed using APP/PS1 mice. We conducted HE staining, ELISA assay, Golgi staining, and immunohistochemistry to detect the protective effect of NP. Additionally, cell experiments were performed to assess cell activity and target protein expression.

resultsNetwork pharmacology analysis revealed 145 drug-disease interactions and identified 5 core active targets associated with AD. Molecular docking results demonstrated strong binding affinity between the components of the NP formula (GP, GN-Rb1, GN-Rg1, NS-R1) and target proteins (STAT3, HIF1A, TLR4, mTOR, VEGFA). Notably, the binding energy between NS-R1 and mTOR was -11.4kcal/mol. Among the top 10 enriched KEGG pathways, the HIF-1 and PI3K-AKT signaling pathways were highlighted.

conclusionOur findings suggest that NP exhibits neuroprotective effects during the early stages of AD, positioning it as a potential candidate for AD prevention. The NP formula may exert its preventive effects through the HIF-1/PI3K-AKT signaling pathway, with mTOR identified as a key target.

Indexed as

Alzheimer DiseaseIridoidsNeuroprotective AgentsProto-Oncogene Proteins c-aktSaponinsSignal TransductionAnimalsDisease Models, AnimalHumansHypoxia-Inducible Factor 1Hypoxia-Inducible Factor 1, alpha SubunitMiceMolecular Docking SimulationNetwork PharmacologyPanax notoginsengPhosphatidylinositol 3-KinasesgeniposideHypoxia-Inducible Factor 1Hypoxia-Inducible Factor 1, alpha SubunitIridoidsNeuroprotective AgentsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSaponinsAlzheimer's diseaseAβgeniposideHIF-1 signaling pathwayPanax notoginseng saponinsPI3K-AKT signaling pathway.

Identifiers

PMID38676511
OpenAlexW4395695181

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.