Evidence map›Paper›PMID 31697645›Full record

ArticleAging2019

Neuroprotective effects of protocatechuic aldehyde through PLK2/p-GSK3β/Nrf2 signaling pathway in both

Chao Guo, Junrong Zhu, Jingwen Wang, Jialin Duan, Shanbo Ma, Ying Yin, Wei Quan, Wei Zhang, Yue Guan, Yi Ding and 2 more

Open access · greenAbstract read
In one paragraph

Article in Aging, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

28 citing papers in PubMed, 48 citations in OpenAlex.

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  6. Neuroprotective Effects and Mechanisms ofInternational journal of molecular sciences · 2025
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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 4 institutions in 1 country.

Chao GuoSchool of Basic Medicine and Clinical Pharmacy, China Pharmaceutical University, Nanjing 211198, China.
Junrong ZhuNanjing First Hospital, China Pharmaceutical University, Nanjing 211198, China.
Jingwen WangDepartment of Pharmacy, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, China.
Jialin DuanDepartment of Pharmacy, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, China.
Shanbo MaDepartment of Pharmacy, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, China.
Ying YinDepartment of Pharmacy, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, China.
Wei QuanMental Health Center, Department of Medicine, Xi'an Jiaotong University, Xi'an 710199, China.
Wei ZhangDepartment of Pharmacy, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, China.
Yue GuanDepartment of Pharmacy, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, China.
Yi DingDepartment of Pharmacy, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, China.
Aidong WenDepartment of Pharmacy, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, China.
Yingdong ZhangNanjing First Hospital, China Pharmaceutical University, Nanjing 211198, China.
Air Force Medical University · CNXijing Hospital · CNChina Pharmaceutical University · CNXi'an Jiaotong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondrial dysfunction and oxidative damage are closely related to the pathogenesis of Parkinson's disease (PD). The pharmacological mechanism of protocatechuic aldehyde (PCA) for PD treatment have retained unclear. The purposes of the present study were to clarify the neuroprotective effects of post-treatment of PCA for PD treatment by mitigating mitochondrial dysfunction and oxidative damage, and to further determine whether its effects were mediated by the polo-like kinase 2/phosphorylated glycogen synthase kinase 3 β/nuclear factor erythroid-2-related factor 2 (PLK2/p-GSK3β/Nrf2) pathways. We found that PCA improved 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP)-induced behavioral deficits and dopaminergic cell loss. Moreover, PCA increased the expressions of PLK2, p-GSK3β and Nrf2, following the decrease of α-synuclein (α-Syn) in MPTP-intoxicated mice. Cell viability was increased and the apoptosis rate was reduced by PCA in 1-methyl-4-phenylpyridinium iodide (MPP

Indexed as

AnimalsApoptosisBenzaldehydesCatecholsCell Line, TumorDisease Models, AnimalDopaminergic NeuronsDrug Evaluation, PreclinicalGlycogen Synthase Kinase 3 betaHumansMaleMice, Inbred C57BLMitochondriaNeuroprotective AgentsNF-E2-Related Factor 2Parkinson DiseaseBenzaldehydesCatecholsGlycogen Synthase Kinase 3 betaNeuroprotective AgentsNfe2l2 protein, mouseNF-E2-Related Factor 2Protein Serine-Threonine Kinasesprotocatechualdehydeserum-inducible kinasemitochondrial dysfunctionParkinson's diseasePLK2-Nrf2 pathwayprotocatechuic aldehydereactive oxygen species

Identifiers

PMID31697645
PMCPMC6874433
OpenAlexW2983175605

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.