Evidence map›Paper›PMID 26648122›Full record

ArticleMolecular medicine reports2016

Calycosin‑7‑O‑β‑D‑glucoside attenuates ischemia‑reperfusion injury in vivo via activation of the PI3K/Akt pathway.

Min Ren, Xudong Wang, Guoqing Du, Jiawei Tian, Yujie Liu

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing 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

21 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. The Study of the Protection Mechanism of Calycosin-7-Molecules (Basel, Switzerland) · 2025
    Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. RSC advances · 2019
    Article
  16. Article
  17. Calycosin-7-Neural plasticity · 2019
    Article
  18. Article
  19. Article
  20. 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 at 2 institutions in 1 country.

Min RenDepartment of Medical Ultrasonics, The Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150086, P.R. China.
Xudong WangDepartment of Medical Ultrasonics, The Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150086, P.R. China.
Guoqing DuDepartment of Medical Ultrasonics, The Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150086, P.R. China.
Jiawei TianDepartment of Medical Ultrasonics, The Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150086, P.R. China.
Yujie LiuDepartment of Medical Ultrasonics, The Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150086, P.R. China.
Harbin Medical University · CNSecond Affiliated Hospital of Harbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The aim of the present study was to investigate the effects and mechanisms of calycosin‑7‑O‑β‑D‑glucoside (CG) on ischemia‑reperfusion (I/R) injury in vivo. Hemodynamic parameters, including ejection fraction (EF), fractional shortening (FS), left ventricular end‑systolic pressure (LVESP) and left ventricular end‑diastolic pressure (LVEDP) were monitored using an ultrasound system, and infarct size was measured using Evans blue/tetrazolium chloride double staining. The activities of serum creatine kinase (CK), lactate dehydrogenase (LDH) and superoxide dismutase (SOD), and the levels of malondialdehyde (MDA) were determined to assess the degree of myocardial injury and oxidative stress‑induced damage. The protein expression levels of cleaved‑caspase‑3, cleaved‑caspase‑9, phosphorylated (p)‑phosphatidylinositol 3‑kinase (PI3K) p85, PI3K p85, p‑Akt and Akt were determined using western blotting. The results demonstrated that pretreatment with high dose (H)‑CG markedly improved cardiac function, as evidenced by upregulated EF, FS and LVESP, and downregulated LVEDP. In addition, administration of CG resulted in significant decreases in infarct size in the I/R+low dose‑CG and I/R+H‑CG groups, compared with the I/R group. The activities of CK and LDH, and the levels of MDA in the I/R+H‑CG group were reduced, compared with those in the I/R group, whereas SOD activity was elevated. Treatment with CG inhibited the cleavage and activity of caspase‑3 and caspase‑9, and enhanced the phosphorylation of PI3K p85 and Akt. Notably, administration of the PI3K inhibitor, LY294002, markedly lowered the levels of p‑PI3K p85/p‑Akt, and eradicated the inhibitory effects of H‑CG on infarct size, myocardial injury and oxidative stress‑induced damage. Taken together, the results suggested that CG may alleviate I/R injury by activating the PI3K/Akt signaling pathway.

Indexed as

AnimalsApoptosisChromonesCreatine KinaseEnzyme ActivationGlucosidesIsoflavonesL-Lactate DehydrogenaseMaleMorpholinesMyocardial InfarctionMyocardial Reperfusion InjuryOxidative StressPhosphatidylinositol 3-KinasePhosphorylationProto-Oncogene Proteins c-akt2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-onecalycosin-7-O-beta-D-glucosideChromonesCreatine KinaseGlucosidesIsoflavonesL-Lactate DehydrogenaseMorpholinesPhosphatidylinositol 3-KinaseProto-Oncogene Proteins c-akt

Identifiers

PMID26648122
PMCPMC4686071
OpenAlexW2178173976

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.