Evidence map›Paper›PMID 26309539›Full record

ArticleInternational journal of clinical and experimental medicine2015

Apigenin attenuates acute myocardial infarction of rats via the inhibitions of matrix metalloprotease-9 and inflammatory reactions.

Hong Du, Jie Hao, Fan Liu, Jingchao Lu, Xiuchun Yang

Abstract read
In one paragraph

Article in International journal of clinical and experimental medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

16 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Article
  3. Neutrophil degranulation and myocardial infarction.Cell communication and signaling : CCS · 2022
    Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Apigenin Alleviates Myocardial Reperfusion Injury in Rats by Downregulating miR-15b.Medical science monitor : international medical journal of experimental and clinical research · 2019
    Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. 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

5 authors at 1 institution in 1 country.

Hong DuDepartment of Cardiology, Second Hospital of Hebei Medical University Shijiazhuang, Hebei, China.
Jie HaoDepartment of Cardiology, Second Hospital of Hebei Medical University Shijiazhuang, Hebei, China.
Fan LiuDepartment of Cardiology, Second Hospital of Hebei Medical University Shijiazhuang, Hebei, China.
Jingchao LuDepartment of Cardiology, Second Hospital of Hebei Medical University Shijiazhuang, Hebei, China.
Xiuchun YangDepartment of Cardiology, Second Hospital of Hebei Medical University Shijiazhuang, Hebei, China.
Hebei Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute myocardial infarction (AMI) is the myocardial necrosis caused by coronary artery acute and persistent ischemia and hypoxia. Matrix metalloprotease-9 (MMP-9) plays an important role in a series of process of occurrence and development of AMI. Inflammatory reaction plays the key role in all kinds of damage factors in AMI. Apigenin (API) has effectively restrained the activity of MMP-9, anti-inflammatory and hepatic fat oxidizing properties. API significantly improved AMI of rats through inhibiting MMP-9 and inflammatory reactions in a few recent studies. Our investigation detected the infarct size of AMI rats, casein kinase (CK), the MB isoenzyme of creatine kinase (CK-MB) and lactate dehydrogenase (LDH) and cardiac troponin T (cTnT) activities in AMI rats were also analyzed with commercial kits. Additionally, Nuclear factor kappa B (NF-κB), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6) levels of whole bloods of AMI rats were also detected using commercial kits. Next, MMP-9 protein of cardiac in AMI rats was measured with gelatin zymography assays. Finally, caspase-3 and caspase-9 activities in AMI rats were analyzed with commercial kits. In the present study, our work indicated API might significantly reduce the infarction size of AMI rat. It was shown that the treatment of API could decrease the expression of MMP-9 level and reduce the activities of NF-κB, TNF-α, IL-1β and IL-6 in AMI rats. Next, API treatment could reduce caspase-3 and caspase-9 activities and decrease cellular apoptosis of AMI rats. Our findings concluded that API ameliorates acute myocardial infarction of rats via inhibiting MMP-9 and inflammatory reactions.

Indexed as

acute myocardial infarctionApigeninapoptosisinflammatoryMMP-9

Identifiers

PMID26309539
PMCPMC4538101
OpenAlexW2419162579

What OpenQuestion 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 OpenQuestion graph.