Evidence map›Paper›PMID 31885818›Full record

ArticleOxidative medicine and cellular longevity2019

FA-97, a New Synthetic Caffeic Acid Phenethyl Ester Derivative, Protects against Oxidative Stress-Mediated Neuronal Cell Apoptosis and Scopolamine-Induced Cognitive Impairment by Activating Nrf2/HO-1 Signaling.

Ting Wan, Zihao Wang, Yi Luo, Yifan Zhang, Wei He, Yu Mei, Jincheng Xue, Min Li, Huafeng Pan, Weirong Li and 2 more

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
3.5field-weighted citation impact, top 6% 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

44 citing papers in PubMed, 88 citations in OpenAlex.

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  20. Molecular Mechanisms of Oxidative Stress Relief by CAPE in ARPE-19 Cells.International journal of molecular sciences · 2023
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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

12 authors at 2 institutions in 2 countries.

Ting WanScience and Technology Innovation Center, Guangzhou University of Chinese Medicine, Guangzhou 510405, China.
Zihao WangInstitute of Brain and Gut Axis (IBAG), Centre of Clinical Research for Chinese Medicine, School of Chinese Medicine, Hong Kong Baptist University, Kowloon Tong, Hong Kong SAR, China.
Yi LuoScience and Technology Innovation Center, Guangzhou University of Chinese Medicine, Guangzhou 510405, China.ORCID https://orcid.org/0000-0001-8452-9523
Yifan ZhangScience and Technology Innovation Center, Guangzhou University of Chinese Medicine, Guangzhou 510405, China.
Wei HeScience and Technology Innovation Center, Guangzhou University of Chinese Medicine, Guangzhou 510405, China.
Yu MeiScience and Technology Innovation Center, Guangzhou University of Chinese Medicine, Guangzhou 510405, China.ORCID https://orcid.org/0000-0001-7378-9880
Jincheng XueScience and Technology Innovation Center, Guangzhou University of Chinese Medicine, Guangzhou 510405, China.
Min LiClinical Medical College of Acupuncture Moxibustion and Rehabilitation, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510006, China.
Huafeng PanScience and Technology Innovation Center, Guangzhou University of Chinese Medicine, Guangzhou 510405, China.
Weirong LiScience and Technology Innovation Center, Guangzhou University of Chinese Medicine, Guangzhou 510405, China.ORCID https://orcid.org/0000-0002-3878-8724
Qi WangScience and Technology Innovation Center, Guangzhou University of Chinese Medicine, Guangzhou 510405, China.ORCID https://orcid.org/0000-0002-3389-8529
Yujie HuangScience and Technology Innovation Center, Guangzhou University of Chinese Medicine, Guangzhou 510405, China.ORCID https://orcid.org/0000-0002-0197-3774
Guangzhou University of Chinese Medicine · CNHong Kong Baptist University · HK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is an age-related neurodegenerative disorder with cognitive deficits, which is becoming markedly more common in the world. Currently, the exact cause of AD is still unclear, and no curative therapy is available for preventing or mitigating the disease progression. Caffeic acid phenethyl ester (CAPE), a natural phenolic compound derived from honeybee hive propolis, has been reported as a potential therapeutic agent against AD, while its application is limited due to the low water solubility and poor bioavailability. Here, caffeic acid phenethyl ester 4-

Indexed as

Alzheimer DiseaseAnimalsApoptosisCaffeic AcidsCognitive DysfunctionDisease Models, AnimalGlucosidesHeme Oxygenase-1HumansMaleMiceMice, Inbred StrainsNeuronsNeuroprotective AgentsNF-E2-Related Factor 2Oxidative Stresscaffeic acid phenethyl esterCaffeic AcidsGlucosidesHeme Oxygenase-1Neuroprotective AgentsNF-E2-Related Factor 2Phenylethyl AlcoholRNA, Small InterferingScopolamine

Identifiers

PMID31885818
PMCPMC6914945
OpenAlexW2990279411

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.