Evidence map›Paper›PMID 41038936›Full record

ArticleScientific reports2025

Indobufen alleviates apoptosis by the PI3K/Akt/eNOS pathway in myocardial ischemia‒reperfusion (I/R) injury.

Kai Hou, Ke Pan, Dan Xu, Yunman Li, Hailong Cao

Abstract read
PubMed Full text at PMC Publisher
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. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Review
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

5 authors.

Kai Hou *Department of Pharmacy, Zhongda Hospital, Southeast University, Nanjing, 210009, China.
Ke Pan *Department of Cardiac Surgery, Zhongda Hospital, Southeast University, Nanjing, 210009, China.
Dan XuState Key Laboratory of Natural Medicines, School of Basic Medical Sciences and Clinical Pharmacy, China Pharmaceutical University, Nanjing, 210009, China.
Yunman LiState Key Laboratory of Natural Medicines, School of Basic Medical Sciences and Clinical Pharmacy, China Pharmaceutical University, Nanjing, 210009, China. yunmanlicpu@163.com.
Hailong CaoDepartment of Cardiac Surgery, Zhongda Hospital, Southeast University, Nanjing, 210009, China. 13675186233@163.com.

Funding

China Pharmaceutical University "Double First-Class" Construction Technology Innovation Team Project CPU2018GY23Hospital Pharmaceutical Research Fund of ChangZhou SiYao,Nanjing Pharmaceutical Association 2022YX003National Science and Technology Major Project of the Ministry of Science and Technology of China 2016ZX09101031
6 · The paper itself

Abstract

Indobufen is a potential antiplatelet drug; the aim of this study was to investigate the pharmacodynamic effects and potential mechanisms of indobufen in a myocardial ischemia/reperfusion (I/R) injury rat model, providing another effective option for the pharmacological prevention of myocardial infarction. In the in vivo model, rats were orally administered indobufen daily. On the fifth day, after 30 min of occlusion of the left anterior descending coronary artery, the rats were reperfused for 2 h. In the in vitro model, the drug was incubated with H9C2 cells for 24 h before the establishment of an oxygen-glucose deprivation/reperfusion (OGD/R) model. Then, the hearts of the rats were collected for TTC staining and myocardial histopathological examination. Creatine kinase (CK), lactate dehydrogenase (LDH), malondialdehyde (MDA), and superoxide dismutase (SOD) levels in rat plasma and cell supernatants were detected with the appropriate kits. Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) and apoptosis-related proteins were used to assess myocardial apoptosis. Western blotting, immunohistochemistry or immunofluorescence were used to detect the expression of p-Akt/Akt and p-eNOS/eNOS. Our results suggest that indobufen ameliorates I/R injury by reducing infarct size, attenuating oxidative stress injury, and inhibiting cardiomyocyte apoptosis. In addition, indobufen increased the expression of p-Akt and p-eNOS in myocardial tissues and H9C2 cells, and LY294002, a specific inhibitor of the PI3K pathway, reversed these protective effects. In conclusion, indobufen reduced myocardial apoptosis and oxidative stress by the PI3K/Akt/eNOS pathway, thereby attenuating MI/R injury and improving cardiac function.

Indexed as

ApoptosisMyocardial Reperfusion InjuryNitric Oxide Synthase Type IIIPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionAnimalsCell LineDisease Models, AnimalMaleMyocardial InfarctionMyocardiumMyocytes, CardiacOxidative StressRatsRats, Sprague-DawleyNitric Oxide Synthase Type IIINos3 protein, ratPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktIndobufenIschemia‒reperfusion (I/R) injuryMyocardial apoptosisMyocardial protectionOxidative stress injuryPI3K/Akt/eNOS pathway

Identifiers

PMID41038936
PMCPMC12491498

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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.