Evidence map›Paper›PMID 34439457›Full record

ArticleAntioxidants (Basel, Switzerland)2021

Supplemental Ferulic Acid Inhibits Total Body Irradiation-Mediated Bone Marrow Damage, Bone Mass Loss, Stem Cell Senescence, and Hematopoietic Defect in Mice by Enhancing Antioxidant Defense Systems.

Sajeev Wagle, Hyun-Jaung Sim, Govinda Bhattarai, Ki-Choon Choi, Sung-Ho Kook, Jeong-Chae Lee, Young-Mi Jeon

Abstract read
In one paragraph

Article in Antioxidants (Basel, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing 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

19 citing papers in PubMed.

  1. Review
  2. Article
  3. Deinoxanthin Recovers HAntioxidants (Basel, Switzerland) · 2025
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  6. Review
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  9. The Role of Zuo Jin Wan in Modulating the Tumor Microenvironment of Colorectal Cancer.Combinatorial chemistry & high throughput screening · 2025
    Article
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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

7 authors.

Sajeev WagleCluster for Craniofacial Development and Regeneration Research, Institute of Oral Bioscience, Jeonbuk National University School of Dentistry, Jeonju 54896, Korea.
Hyun-Jaung SimCluster for Craniofacial Development and Regeneration Research, Institute of Oral Bioscience, Jeonbuk National University School of Dentistry, Jeonju 54896, Korea.
Govinda BhattaraiCluster for Craniofacial Development and Regeneration Research, Institute of Oral Bioscience, Jeonbuk National University School of Dentistry, Jeonju 54896, Korea.
Ki-Choon ChoiGrassland and Forages Research Center, National Institute of Animal Science, Cheonan 31002, Korea.ORCID 0000-0001-8071-5097
Sung-Ho KookCluster for Craniofacial Development and Regeneration Research, Institute of Oral Bioscience, Jeonbuk National University School of Dentistry, Jeonju 54896, Korea.
Jeong-Chae LeeCluster for Craniofacial Development and Regeneration Research, Institute of Oral Bioscience, Jeonbuk National University School of Dentistry, Jeonju 54896, Korea.
Young-Mi JeonCluster for Craniofacial Development and Regeneration Research, Institute of Oral Bioscience, Jeonbuk National University School of Dentistry, Jeonju 54896, Korea.

Funding

National Research Foundation of Korea 2018R1D1A1B07046563National Research Foundation of Korea 2020R1C1C1004968National Research Foundation of Korea 2021R111A1A01044453National Research Foundation of Korea 2021R1A2C2006032Rural Development Administration PJ013394022021
6 · The paper itself

Abstract

While total body irradiation (TBI) is an everlasting curative therapy, the irradiation can cause long-term bone marrow (BM) injuries, along with senescence of hematopoietic stem cells (HSCs) and mesenchymal stem cells (MSCs) via reactive oxygen species (ROS)-induced oxidative damages. Thus, ameliorating or preventing ROS accumulation and oxidative stress is necessary for TBI-requiring clinical treatments. Here, we explored whether administration of ferulic acid, a dietary antioxidant, protects against TBI-mediated systemic damages, and examined the possible mechanisms therein. Sublethal TBI (5 Gy) decreased body growth, lifespan, and production of circulating blood cells in mice, together with ROS accumulation, and senescence induction of BM-conserved HSCs and MSCs. TBI also impaired BM microenvironment and bone mass accrual, which was accompanied by downregulated osteogenesis and by osteoclastogenic and adipogenic activation in BM. Long-term intraperitoneal injection of ferulic acid (50 mg/kg body weight, once per day for 37 consecutive days) protected mice from TBI-mediated mortality, stem cell senescence, and bone mass loss by restoring TBI-stimulated disorders in osteogenic, osteoclastic, and adipogenic activation in BM. In vitro experiments using BM stromal cells supported radioprotective effects of ferulic acid on TBI-mediated defects in proliferation and osteogenic differentiation. Overall, treatment with ferulic acid prevented TBI-mediated liver damage and enhanced endogenous antioxidant defense systems in the liver and BM. Collectively, these results support an efficient protection of TBI-mediated systemic defects by supplemental ferulic acid, indicating its clinical usefulness for TBI-required patients.

Indexed as

antioxidant defense systembone marrow injurybone marrow microenvironmentferulic acidreactive oxygen speciesstem cell senescencetotal body irradiation

Identifiers

PMID34439457
PMCPMC8388974

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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.