Evidence map›Paper›PMID 39017801›Full record

ArticleMolecular biology reports2024

The protective effect of parthenolide in an in vitro model of Parkinson's disease through its regulation of nuclear factor-kappa B and oxidative stress.

Seyed Ali Shariat Razavi, Farzane Vafaei, Seyyed Moein Ebrahimi, Farzaneh Abbasinezhad-Moud, Ali Shahini, Farid Qoorchi Moheb Seraj, Mohaddeseh Sadat Alavi, Arghavan Fadavieslam, Gordon A Ferns, Afsane Bahrami

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Article in Molecular biology reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

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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

2 citing papers in PubMed.

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4 · The record

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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

10 authors.

Seyed Ali Shariat Razavi *Neurosurgery Department, Ghaem Hospital, Mashhad University of Medical Sciences, Mashhad, Iran.
Farzane Vafaei *Department of Pharmacy, Shahreza Branch, Islamic Azad University, Shahreza, Isfahan, PO 311-86145, Iran.
Seyyed Moein Ebrahimi *Department of Biochemistry, Faculty of Medicine, Gonabad University of Medical Sciences, Gonabad, Iran.
Farzaneh Abbasinezhad-MoudDepartment of Medical Biochemistry, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
Ali ShahiniFaculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
Farid Qoorchi Moheb SerajEndovascular Section, Neurosurgical Department, Ghaem Hospital, Mashhad University of Medical Sciences, Mashhad, Iran.
Mohaddeseh Sadat AlaviDepartment of Pharmacology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
Arghavan FadavieslamDepartment of Medical Biochemistry, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
Gordon A FernsDivision of Medical Education, Brighton & Sussex Medical School, Falmer, Brighton, Sussex, BN1 9PH, UK.
Afsane BahramiClinical Research Development Unit, Faculty of Medicine, Imam Reza Hospital, Mashhad University of Medical Sciences, Mashhad, Iran. Afsbahramia931@gmail.com.

Funding

Mashhad University of M 4020025
6 · The paper itself

Abstract

backgroundParkinson's disease (PD) is a neurodegenerative disorder characterized by motor and non-motor symptoms, and is due to the degeneration of dopaminergic neurons. It is multifactorial, caused by genetic and environmental factors and currently has no definitive cure. We have investigated the protective effects of parthenolide (PTN), a compound with known anti-inflammatory and antioxidant properties, in an in vitro model of PD, that is induced by 6-OHDA, and that causes neurotoxicity in SH-SY5Y human neuroblastoma cells. METHODS AND

resultsSH-SY5Y cells were pretreated with PTN to assess its protective effects in 6-OHDA-induced cellular damage. Cell viability was measured using Alamar blue. Apoptosis was evaluated using an Annexin V-FITC/PI kit. Reactive oxygen species (ROS) levels were quantified, and expression levels of apoptotic markers (Bax, Bcl-2, p53) and NF-κB were analyzed via Western blotting and Quantitative real-time- (qRT-) PCR. We found that 6-OHDA reduced cell viability, that was inhibited significantly by pre-treatment with PTN (p < 0.05). Flow cytometry revealed that PTN reduced apoptosis induced by 6-OHDA. PTN also reduced the ROS levels raised by 6-OHDA (p < 0.05). Moreover, PTN decreased the expression of Bax, p53, NF-κB, and p-NF-κB that were increased by treatment with 6-OHDA.

conclusionThese findings indicate the potential beneficial effects of PTN in an in vitro model of PD via mitigating oxidative stress and inflammation, suggested PTN as a promising agent to be used for PD therapy, warranting further investigation in preclinical and clinical studies.

Indexed as

ApoptosisCell SurvivalNF-kappa BOxidative StressOxidopamineParkinson DiseaseReactive Oxygen SpeciesSesquiterpenesAntioxidantsCell Line, TumorHumansNeuroprotective AgentsAntioxidantsNeuroprotective AgentsNF-kappa BOxidopamineparthenolideReactive Oxygen SpeciesSesquiterpenes6-HydroxydopamineNeuroprotectionOxidative stressParkinson's diseaseParthenolide

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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 Socratic graph.