Evidence map›Paper›PMID 39458526›Full record

ArticleNutrients2024

Dietary Probiotic

Jaung-Geng Lin, Wen-Ping Jiang, You-Shan Tsai, Shih-Wei Lin, Yen-Lien Chen, Chin-Chu Chen, Guan-Jhong Huang

Abstract read
In one paragraph

Article in Nutrients, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 1 pooled it
–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

6 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Cisplatin-Induced Nephrotoxicity Attenuation byInternational journal of molecular sciences · 2026
    Article
  4. The Brown Strain ofInternational journal of molecular sciences · 2026
    Article
  5. Microbiota-gut-kidney axis in health and renal disease.International journal of biological sciences · 2026
    Review
  6. Whole Genome Analysis ofAntibiotics (Basel, Switzerland) · 2025
    Article
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.

Jaung-Geng LinSchool of Chinese Medicine, College of Chinese Medicine, China Medical University, Taichung 404, Taiwan.ORCID 0000-0002-3642-8047
Wen-Ping JiangSchool of Pharmacy, College of Pharmacy, China Medical University, Taichung 404, Taiwan.
You-Shan TsaiBiotech Research Institute, Grape King Bio Ltd., Taoyuan City 325, Taiwan.ORCID 0000-0002-9585-2219
Shih-Wei LinBiotech Research Institute, Grape King Bio Ltd., Taoyuan City 325, Taiwan.
Yen-Lien ChenBiotech Research Institute, Grape King Bio Ltd., Taoyuan City 325, Taiwan.
Chin-Chu ChenInstitute of Food Science and Technology, National Taiwan University, Taipei 106, Taiwan.
Guan-Jhong HuangDepartment of Food Nutrition and Healthy Biotechnology, Asia University, Taichung 413, Taiwan.ORCID 0000-0002-9822-3485

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND/

objectivesAcute kidney injury (AKI) syndrome is distinguished by a quick decline in renal excretory capacity and usually diagnosed by the presence of elevated nitrogen metabolism end products and/or diminished urine output. AKI frequently occurs in hospital patients, and there are no existing specific treatments available to diminish its occurrence or expedite recovery. For an extended period in the food industry,

methodsIn this study, the aim is to assess the effectiveness of

resultsThe findings indicated the significant alleviation of the renal histopathological changes and serum biomarkers of GKA4, dead probiotic GKA4, and postbiotic GKA4 in cisplatin-induced nephrotoxicity. GKA4, dead probiotic GKA4, and postbiotic GKA4 elevated the expression levels of HO-1 and decreased the expression levels of Nrf-2 proteins. In addition, the administration of GKA4, dead probiotic GKA4, and postbiotic GKA4 significantly reduced the expression of apoptosis-related proteins (Bax, Bcl-2, and caspase 3), autophagy-related proteins (LC3B, p62, and Beclin1), and endoplasmic reticulum (ER) stress-related proteins (GRP78, PERK, ATF-6, IRE1, CHOP, and Caspase 12) in kidney tissues. Notably, GKA4, dead probiotic GKA4, and postbiotic GKA4 also upregulated the levels of proteins related to organic anion transporters and organic cation transporters.

conclusionsOverall, the potential therapeutic benefits of GKA4, dead probiotic GKA4, and postbiotic GKA4 are significant, particularly after cisplatin treatment. This is achieved by modulating apoptosis, autophagy, ER stress, and transporter proteins to alleviate oxidative stress.

Indexed as

Acute Kidney InjuryAutophagyCisplatinEndoplasmic Reticulum Chaperone BiPEndoplasmic Reticulum StressPediococcus acidilacticiProbioticsAnimalsApoptosisDisease Models, AnimalKidneyMaleMiceOrganic Anion TransportersCisplatinEndoplasmic Reticulum Chaperone BiPHspa5 protein, mouseOrganic Anion Transportersacute kidney injuryapoptosisautophagycisplatinER stressoxidative stressPediococcus acidilactici GKA4transporter proteins

Identifiers

PMID39458526
PMCPMC11510457

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Registered trials

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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.