Evidence map›Paper›PMID 42319576›Full record

ArticleMolecular biology reports2026

Neuroprotective effects of gallic acid in an MPP⁺-induced SH-sy5y cell model of parkinson's disease.

Hasan Ulusal, Hatice Kubra Yigit Dumrul, Sibel Dagli, Mustafa Oztatlici, Mehmet Tarakcioglu

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular biology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

5 authors.

Hasan UlusalDepartment of Medical Biochemistry, Faculty of Medicine, Gaziantep Islam Science and Technology University, 27010, Gaziantep, Turkey. hasan.ulusal@gibtu.edu.tr.ORCID http://orcid.org/0000-0003-3890-2088
Hatice Kubra Yigit DumrulDepartment of Physiology, Faculty of Medicine, Agri İbrahim Cecen University, 04100, Agri, Turkey.ORCID http://orcid.org/0000-0002-6780-229X
Sibel DagliDepartment of Medical Microbiology, Faculty of Medicine, Sanko University, Gaziantep, 27000, Turkey.ORCID http://orcid.org/0000-0003-0596-4178
Mustafa OztatliciDepartment of Histology and Embryology, Faculty of Medicine, Gaziantep Islam Science and Technology University, 27010, Gaziantep, Turkey.ORCID http://orcid.org/0000-0001-9914-7122
Mehmet TarakciogluDepartment of Medical Biochemistry, Faculty of Medicine, Gaziantep University, 27310, Gaziantep, Turkey.ORCID http://orcid.org/0000-0002-2398-8264

Funding

Gaziantep Üniversitesi TF.HZP.23.44
6 · The paper itself

Abstract

backgroundParkinson's Disease (PD) represents the second most prevalent neurodegenerative condition which leads to the progressive destruction of dopaminergic neurons in the substantia nigra through oxidative stress mechanisms. The research evaluated Gallic Acid (GA) as a natural polyphenol with proven antioxidant properties for its ability to protect cells from 1-methyl-4-phenylpyridinium (MPP⁺)-induced neurotoxicity in SH-SY5Y dopaminergic cell models.

methodsThe research used SH-SY5Y cells which received 1 mM MPP⁺ treatment alongside different GA concentrations (25, 50 and 100 µM) for 24 and 48 h. The CCK-8 assay measured cell viability while flow cytometry evaluated apoptosis and SOD and MDA levels determined oxidative status through SOD and Catalase and NO measurements.

resultsThe addition of MPP⁺ resulted in a 32.74% decrease in cell viability at 48 h while simultaneously decreasing SOD and Catalase and NO levels and increasing MDA levels. The addition of 25 µM GA protected cells from damage by increasing their viability to 86.53% at 48 h and decreasing apoptotic cell numbers. Our results revealed that co-treatment with 25-50 µM GA effectively mitigated oxidative damage by preventing the depletion of catalase and NO levels. Furthermore, GA successfully reduced lipid peroxidation; specifically, 25 µM GA decreased MDA levels from 21.18 to 9.64 nM/mg protein at 48 h, thereby restoring the cellular antioxidant defense system against MPP

conclusionsIn conclusion, the present study demonstrates that GA exerts a significant neuroprotective effect in an in vitro PD model by modulating the endogenous antioxidant network and alleviating lipid peroxidation. By effectively reversing the depletion of crucial enzymes and reducing apoptosis, GA shows potential therapeutic efficacy against oxidative stress-associated neurodegeneration. These findings suggest that GA is a promising phytochemical candidate warranting further in vivo evaluation to clarify its long-term bioavailability and translational value.

Indexed as

Gallic AcidNeuroprotective AgentsParkinson Disease1-Methyl-4-phenylpyridiniumAntioxidantsApoptosisCatalaseCell Line, TumorCell SurvivalDopaminergic NeuronsHumansLipid PeroxidationOxidative StressSuperoxide Dismutase1-Methyl-4-phenylpyridiniumAntioxidantsCatalaseGallic AcidNeuroprotective AgentsSuperoxide DismutaseApoptosisGallic acidMPP+NeuroprotectionOxidative Stress

Identifiers

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.