Evidence map›Paper›PMID 31015891›Full record

ArticleOxidative medicine and cellular longevity2019

Nutritional Preconditioning of Apigenin Alleviates Myocardial Ischemia/Reperfusion Injury via the Mitochondrial Pathway Mediated by Notch1/Hes1.

Huang Huang, Songqing Lai, Yong Luo, Qing Wan, Qicai Wu, Li Wan, Wanghong Qi, Jichun Liu

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2019. 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
2.7field-weighted citation impact, top 11% of its field
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, 32 citations in OpenAlex.

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  14. Hematogenous Macrophages: A New Therapeutic Target for Spinal Cord Injury.Frontiers in cell and developmental biology · 2021
    Review
  15. Article
  16. Review
  17. Article
  18. Remedying the Mitochondria to Cure Human Diseases by Natural Products.Oxidative medicine and cellular longevity · 2020
    Review
  19. 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

8 authors at 2 institutions in 1 country.

Huang HuangDepartment of Cardiac Surgery, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, China.
Songqing LaiDepartment of Cardiac Surgery, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, China.
Yong LuoJiangxi Provincial Key Laboratory of Women's Reproductive Health, Jiangxi Provincial Maternal and Child Health Hospital, Nanchang 330006, China.
Qing WanDepartment of Pharmacy, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, China.
Qicai WuDepartment of Cardiac Surgery, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, China.
Li WanDepartment of Cardiac Surgery, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, China.
Wanghong QiDepartment of Cardiac Surgery, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, China.
Jichun LiuDepartment of Cardiac Surgery, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, China.ORCID 0000-0003-3865-407X
Nanchang University · CNJiangxi Maternal and Child Health Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Apigenin (Api), a natural flavone found in high amounts in several herbs, has shown potent cardioprotective effects in clinical studies, although the underlying mechanisms are not clear. We hypothesized that Api protects the myocardium from simulated ischemia/reperfusion (SI/R) injury via nutritional preconditioning (NPC). Rats fed with Api-containing food showed improvement in cardiac functions; lactate dehydrogenase (LDH) and creatine phosphokinase (CPK) activities; infarct size; apoptosis rates; malondialdehyde (MDA) levels; caspase-3, superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) activities; and ferric reducing antioxidant power (FRAP) compared to those fed standard chow following SI/R injury. In addition, Api pretreatment significantly improved the viability, decreased the LDH activity and intracellular reactive oxygen species (ROS) generation, alleviated the loss of mitochondrial membrane potential (MMP), prevented the opening of the mitochondrial permeability transition pore (mPTP), and decreased the caspase-3 activity, cytochrome c (Cyt C) release, and apoptosis induced by SI/R in primary cardiomyocytes. Mechanistically, Api upregulated Hes1 expression and was functionally neutralized by the Notch1

Indexed as

AnimalsAnimals, NewbornApigeninApoptosisAtractylosideCardiotonic AgentsCell SurvivalLipid PeroxidationMitochondriaMyocardial Reperfusion InjuryMyocardiumMyocytes, CardiacOxidative StressRats, Sprague-DawleyReceptor, Notch1Transcription Factor HES-1ApigeninAtractylosideCardiotonic AgentsHes1 protein, ratReceptor, Notch1Transcription Factor HES-1

Identifiers

PMID31015891
PMCPMC6446095
OpenAlexW2923751886

What OpenQuestion holds

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LicenceCC BY
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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.