Evidence map›Paper›PMID 42009995›Full record

ArticleInflammopharmacology2026

Exploring the role of tocotrienol-rich fraction (TRF) in ameliorating neuroinflammation.

Jing Yi Tan, Thaarvena Retinasamy, Vanessa Lin Lin Lee, Ammu Kutty Radhakrishnan, Keng Yoon Yeong

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

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1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

5 authors.

Jing Yi TanSchool of Science, Monash University Malaysia Campus, Jalan Lagoon Selatan, 47500, Bandar Sunway, Selangor, Malaysia.
Thaarvena RetinasamyNeuropharmacology Research Laboratory, Jeffrey Cheah School of Medicine and Health Sciences, Monash University Malaysia, 47500, Bandar Sunway, Selangor, Malaysia. thaarvena.retinasamy@monash.edu.
Vanessa Lin Lin LeeNeuropharmacology Research Laboratory, Jeffrey Cheah School of Medicine and Health Sciences, Monash University Malaysia, 47500, Bandar Sunway, Selangor, Malaysia.
Ammu Kutty RadhakrishnanFood As Medicine Research Strength, Jeffrey Cheah School of Medicine and Health Sciences, Monash University Malaysia, 47500, Bandar Sunway, Petaling Jaya, Selangor, Malaysia.
Keng Yoon YeongSchool of Science, Monash University Malaysia Campus, Jalan Lagoon Selatan, 47500, Bandar Sunway, Selangor, Malaysia. yeong.kengyoon@monash.edu.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neuroinflammation is a chronic inflammatory response that contributes to synaptic dysfunction and neuronal damage, it is a common feature among various neurodegenerative diseases such as Alzheimer's Disease (AD), Parkinson's Disease (PD) and Huntington's Disease (HD). Tocotrienol-rich fraction (TRF) is a form of vitamin E that is known for its anti-inflammatory, antioxidant and neuroprotective properties. Yet, it has not been adequately investigated in both cellular and animal neuroinflammation models. In this study, the potential therapeutic effects of TRF were investigated in-vitro using BV2 microglial cells and also in-vivo in a pilot study using Sprague Dawley rats. TRF at 5 and 10 µg/mL were found to reduce nitric oxide (NO) and reactive oxygen species (ROS) levels. Furthermore, in-vivo treatment with TRF significantly increases the recognition index implying improvement in cognition ability. Gene expression analysis showed downregulation of RelA, TNF-α and IL-6 while NFE2L2 and BDNF were upregulated. These findings suggests that TRF may help mitigates neuroinflammation and oxidative stress, indicating its potential as a candidature for further investigation in neurodegenerative diseases associated with chronic neuroinflammation.

Indexed as

Anti-Inflammatory AgentsInflammationNeuroinflammatory DiseasesTocotrienolsAnimalsAntioxidantsMaleMiceMicrogliaNeurodegenerative DiseasesNeuroprotective AgentsNitric OxideOxidative StressRatsRats, Sprague-DawleyReactive Oxygen SpeciesAnti-Inflammatory AgentsAntioxidantsNeuroprotective AgentsNitric OxideReactive Oxygen SpeciesTocotrienolsAnti-inflammatoryAntioxidantNeuroinflammationNeuroprotectionTocotrienol-rich fraction (TRF)Vitamin E

Identifiers

PMID42009995
PMCPMC13275581

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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.