Evidence map›Paper›PMID 24922524›Full record

ArticleCNS neuroscience & therapeutics2014

Effect of tacrine-3-caffeic acid, a novel multifunctional anti-Alzheimer's dimer, against oxidative-stress-induced cell death in HT22 hippocampal neurons: involvement of Nrf2/HO-1 pathway.

Xiao-Juan Chao, Zi-Wei Chen, An-Min Liu, Xi-Xin He, Shao-Gui Wang, Yu-Ting Wang, Pei-Qing Liu, Charles Ramassamy, Shing-Hung Mak, Wei Cui and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in CNS neuroscience & therapeutics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

19 citing papers in PubMed, 53 citations in OpenAlex.

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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

14 authors at 6 institutions in 4 countries.

Xiao-Juan ChaoDepartment of Pharmacology & Toxicology, School of Pharmaceutical Sciences, Sun Yat-Sen University, Guangzhou, China.
Zi-Wei Chen
An-Min Liu
Xi-Xin He
Shao-Gui Wang
Yu-Ting Wang
Pei-Qing Liu
Charles Ramassamy
Shing-Hung Mak
Wei Cui
Ah-Ng Kong
Zhi-Ling Yu
Yi-Fan Han
Rong-Biao Pi
Sun Yat-sen University · CNHong Kong Polytechnic University · HKGuangzhou University of Chinese Medicine · CNHong Kong Baptist University · HKInstitut National de la Recherche Scientifique · CARutgers, The State University of New Jersey · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsOxidative stress (OS) plays an important role in the pathogenesis of neurodegenerative diseases, including Alzheimer's disease (AD). This study was designed to uncover the cellular and biochemical mechanisms underlying the neuroprotective effects of tacrine-3-caffeic acid (T3CA), a novel promising multifunctional anti-Alzheimer's dimer, against OS-induced neuronal death. METHODS AND

resultsT3CA protected HT22 cells against high-concentration-glutamate-induced cell death in time- and concentration-dependent manners and potently attenuated glutamate-induced intracellular reactive oxygen species (ROS) production as well as mitochondrial membrane-potential (ΔΨ) disruption. Besides, T3CA significantly induced nuclear factor erythroid 2-related factor 2 (Nrf2) nuclear translocation and increased its transcriptional activity, which were demonstrated by Western blotting, immunofluorescence, and antioxidant response element (ARE)-luciferase reporter gene assay. Further studies showed that T3CA potently up-regulated heme oxygenase-1 (HO-1), an endogenous antioxidative enzyme and a downstream effector of Nrf2, at both mRNA and protein levels. The neuroprotective effects of T3CA were partially reversed by brusatol, which reduced protein level of Nrf2, or by inhibiting HO-1 with siRNA or ZnPP-IX, a specific inhibitor of HO-1.

conclusionsTaken together, these results clearly demonstrate that T3CA protects neurons against OS-induced cell death partially through Nrf2/ARE/HO-1 signaling pathway, which further supports that T3CA might be a promising novel therapeutic agent for OS-associated diseases.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsCaffeic AcidsCell DeathCell Line, TransformedCytoskeletal ProteinsGlutamic AcidHeme Oxygenase-1HumansKelch-Like ECH-Associated Protein 1Membrane Potential, MitochondrialMiceNeuronsNF-E2-Related Factor 2Nootropic AgentsOxidative StressAdaptor Proteins, Signal Transducingcaffeic acidCaffeic AcidsCytoskeletal ProteinsGlutamic AcidHeme Oxygenase-1Keap1 protein, mouseKelch-Like ECH-Associated Protein 1NF-E2-Related Factor 2Nootropic AgentsReactive Oxygen SpeciesRNA, MessengerRNA, Small InterferingTacrineCell deathHO-1Nrf2Oxidative stressT3CA

Identifiers

PMID24922524
PMCPMC6493203
OpenAlexW2097898843

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.