Evidence map›Paper›PMID 41028047›Full record

ArticleScientific reports2025

The therapeutic potential of beta-carotene against neuroinflammation and amyloid beta in SH-SY5Y cells.

Muhammad Imran Khan, Eun Sun Jeong, Gull Tasreen, Muhammad Zubair Khan, Jin Hyuk Shin, Jong Deog Kim

Abstract read
In one paragraph

Article in Scientific reports, 2025. 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

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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

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

6 authors.

Muhammad Imran KhanDepartment of Biotechnology, Faculty of Biomedical and Life Sciences, Kohsar University, Murree, Pakistan.
Eun Sun JeongDepartment of Laboratory Medicine, Yeosu Chonnam Hospital, Yeosu, South Korea.
Gull TasreenDepartment of Biotechnology, Faculty of Science and Technology, Women University of Azad Jammu and Kashmir Bagh, Bagh, Azad Kashmir, Pakistan.
Muhammad Zubair KhanDepartment of Biotechnology, Faculty of Biomedical and Life Sciences, Kohsar University, Murree, Pakistan.
Jin Hyuk ShinDepartment of Biotechnology, Chonnam Notational University, San96-1, Dun-Duk Dong, Yeosu, Chonnam, 59626, South Korea.
Jong Deog KimDepartment of Biotechnology, Chonnam Notational University, San96-1, Dun-Duk Dong, Yeosu, Chonnam, 59626, South Korea. pasteur@jnu.ac.kr.

Funding

National Research Foundation of Korea NRF-2018R1D1A1B07047021
6 · The paper itself

Abstract

Neurodegenerative diseases, particularly Alzheimer's disease (AD), represent a significant public health challenge due to their increasing prevalence and the lack of effective treatments. In this study, we explored the neuroprotective effects of beta-carotene, a naturally occurring carotenoid, by investigating its ability to inhibit or reduce apoptosis and inflammation while enhancing antioxidant potential in SH-SY5Y neuroblastoma cells. Beta-carotene was extracted from Chlorella vulgaris using high-performance liquid chromatography (HPLC). We utilized SH-SY5Y cells, a widely employed in vitro model for studying neurodegenerative processes, to evaluate these therapeutic effects. A combination of colorimetric assays, enzyme-linked immunosorbent assays (ELISA), and quantitative real-time PCR (qRT-PCR) was used to assess the impact of beta-carotene on enzyme activity, cytokine production, and gene expression. The caspase assay results demonstrated that beta-carotene effectively reduced the activity of pro-apoptotic caspases and downregulated the expression of pro-apoptotic genes such as Bax, Bak and caspases, thereby inhibiting apoptosis in SH-SY5Y cells. Additionally, beta-carotene exhibited potent antioxidant properties by upregulating NRF2 and superoxide dismutase (SOD), along with enhancing ABTS and DPPH radical scavenging activities.showed antiinflamatory effects reduce the concentrations of proinflamatory cytokines TNFα, IL-1 β and IFN-γ, and supress the inflamtion patway by supressing the expression of Akt, PIK3, STAT1 and NF-kB, Akt etc. Importantly, beta-carotene treatment led to the suppression of β-secretase (BACE1), γ-secretase and acetylcholinesterase (AChE) activities, and the downregulation of genes involved in amyloid-beta production, including BACE1, and PECN1 eventualy resulted in dcerase concentration o Aβ peptides. These findings suggest that β-carotene could be a promising therapeutic candidate for the prevention and treatment of neurodegenerative diseases, particularly Alzheimer's disease, however further investigations are recomended in animal models and clinical trials before incorporating beta-cerotene into pharmaceutical formulations for AD treatment.

Indexed as

Amyloid beta-Peptidesbeta CaroteneNeuroinflammatory DiseasesNeuroprotective AgentsAlzheimer DiseaseAmyloid Precursor Protein SecretasesAntioxidantsApoptosisCell Line, TumorHumansAmyloid beta-PeptidesAmyloid Precursor Protein SecretasesAntioxidantsbeta CaroteneNeuroprotective AgentsAlzheimer’s diseaseAnti-inflammatoryAntioxidantApoptosisChlorella vulgarisIL-1βNeurodegenerationβ-carotene

Identifiers

PMID41028047
PMCPMC12484793

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LicenceCC BY-NC-ND
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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 OpenQuestion graph.