Evidence map›Paper›PMID 33172292›Full record

ArticleCell transplantation

Glaucocalyxin A Protects H9c2 Cells Against Hypoxia/Reoxygenation-Induced Injury Through the Activation of Akt/Nrf2/HO-1 Pathway.

Zhuo Peng, Rui Zhang, Longfei Pan, Honghong Pei, Zequn Niu, Hai Wang, Junhua Lv, Xiaoyan Dang

Open access · goldAbstract read
In one paragraph

Article in Cell transplantation. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.8field-weighted citation impact, top 30% 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

11 citing papers in PubMed, 15 citations in OpenAlex.

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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 1 institution in 1 country.

Zhuo PengEmergency Department, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi Province, China.
Rui ZhangEmergency Department, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi Province, China.
Longfei PanEmergency Department, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi Province, China.
Honghong PeiEmergency Department, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi Province, China.
Zequn NiuEmergency Department, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi Province, China.
Hai WangEmergency Department, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi Province, China.
Junhua LvEmergency Department, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi Province, China.
Xiaoyan DangEmergency Department, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi Province, China.ORCID 0000-0002-5626-8562
Second Affiliated Hospital of Xi'an Jiaotong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myocardial infarction (MI) is one of the most serious cardiovascular diseases associated with myocardial ischemia/reperfusion (I/R) injury. Glaucocalyxin A (GLA) is a biologically active ent-kauranoid diterpenoid that has been found to ameliorate myocardial I/R injury in mice. However, the mechanism has not been fully investigated. In the present study, we aimed to investigate the effect of GLA on rat cardiomyocytes H9c2 cells exposed to hypoxia/reoxygenation (H/R). The results showed that GLA treatment improved cell viability of H/R-stimulated H9c2 cells. Administration with GLA suppressed the H/R-stimulated reactive oxygen species (ROS) production in H9c2 cells. GLA also elevated the activities of antioxidant enzymes, including superoxide dismutase and glutathione peroxidase in H/R-stimulated H9c2 cells. Moreover, GLA prevented H/R-stimulated cell apoptosis in H9c2 cells, as evidenced by increased bcl-2 expression, decreased bax expression, as well as reduced caspase-3 activity. Furthermore, GLA enhanced the activation of protein kinase B (Akt)/nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) signaling pathway in H9c2 cells exposed to H/R. Additionally, treatment with LY294002 reserved the protective effects of GLA on H/R-stimulated oxidative injury in H9c2 cells. In conclusion, these findings suggested that GLA protected H9c2 cells from H/R-stimulated oxidative damage, which was mediated by the Akt/Nrf2/HO-1 signaling pathway. Thus, GLA might be a promising therapeutic agent for the prevention and treatment of myocardial I/R.

Indexed as

AnimalsBlotting, WesternCell HypoxiaCell SurvivalDiterpenes, KauraneEnzyme-Linked Immunosorbent AssayHeme Oxygenase (Decyclizing)Myocardial Reperfusion InjuryNF-E2-Related Factor 2Oxidative StressRatsReactive Oxygen SpeciesSignal TransductionDiterpenes, Kauraneglaucocalyxin AHeme Oxygenase (Decyclizing)Hmox1 protein, ratNF-E2-Related Factor 2Reactive Oxygen SpeciesAkt/Nrf2/HO-1 signaling pathwayglaucocalyxin A (GLA)myocardial infarction (MI)myocardial ischemia/reperfusion (I/R) injuryoxidative stress

Identifiers

PMID33172292
PMCPMC7784558
OpenAlexW3100979473

What OpenQuestion holds

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LicenceCC BY-NC
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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.