Evidence map›Paper›PMID 41416166›Full record

ArticleSichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition2025

[Mechanism of Trifolin in Attenuating Hypertension-Induced Renal Cell Apoptosis via Modulation of the MAPK Signaling Pathway].

Meizhu Wu, Zhi Guo, Yi Xie, Hongshu Liu, Hong Chen, Xinbiao Lin, Rongji Chen, Aling Shen, Jun Peng

Abstract readEnglish Abstract
In one paragraph

Article in Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition, 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

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

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

9 authors.

Meizhu Wu( 350122) Academy of Integrative Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou 350122, China.ORCID 0000-0003-2010-8644
Zhi Guo( 350122) Academy of Integrative Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou 350122, China.
Yi Xie( 350122) Academy of Integrative Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou 350122, China.
Hongshu Liu( 350122) Academy of Integrative Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou 350122, China.
Hong Chen( 350122) Academy of Integrative Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou 350122, China.
Xinbiao Lin( 350122) Academy of Integrative Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou 350122, China.
Rongji Chen( 350122) Academy of Integrative Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou 350122, China.
Aling Shen( 350122) Academy of Integrative Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou 350122, China.
Jun Peng( 350122) Academy of Integrative Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou 350122, China.ORCID 0000-0003-2010-8644

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objective: To investigate the potential therapeutic effects of trifolin on hypertension-induced renal injury, as well as the key targets and pathways involved. Methods: The mRNA transcriptional profiles of peripheral blood clinical samples from hypertensive patients were analyzed using Gene Expression Omnibus (GEO), a high-throughput gene expression database. The network pharmacology method was employed to screen key targets of trifolin in treating hypertension-induced renal injury. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were conducted. NRK-52E cells, a rat renal proximal tubular cell line, were used to construct an angiotensin Ⅱ (Ang Ⅱ)-stimulated cell model. Flow cytometry was performed to assess cell apoptosis rates and Western blotting was performed to determine the expression levels of apoptosis-related proteins, including Bax, Bcl-2, cleaved caspase-3, and caspase-3, and the phosphorylation and total protein levels of the key MAPK pathway proteins, including ERK, p38 MAPK, and JNK. Results: Analysis of the dataset GSE75360 revealed that, compared with healthy controls, 3331 genes were upregulated and 3197 genes were downregulated in peripheral blood mononuclear cells of hypertensive patients. According to network pharmacology analysis, 472 potential targets of trifolin were identified, including CASP3 and MAPK1. Protein-protein interaction network analysis showed that these targets were closely associated with apoptosis regulatory signaling pathways. GO and KEGG pathway enrichment analyses indicated that trifolin was significantly enriched in pathways associated with negative regulation of apoptosis, apoptotic signaling pathways, and the MAPK signaling pathway. The Conclusion: Trifolin may exert its protective effect against hypertension-induced renal injury by inhibiting Ang Ⅱ-induced NRK-52E cell apoptosis and regulating the MAPK signaling pathway, representing an important mechanism underlying its therapeutic action.

Indexed as

ApoptosisHypertensionMAP Kinase Signaling SystemAngiotensin IIAnimalsCell LineHumansKidneyMaleRatsAngiotensin IICell apoptosisHypertensive nephropathyMAPK signaling pathwayTrifolin

Identifiers

PMID41416166
PMCPMC12709063

What Socratic holds

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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 Socratic graph.