Evidence map›Paper›PMID 32323734›Full record

ArticleInternational journal of molecular medicine2020

Melatonin elicits protective effects on OGD/R‑insulted H9c2 cells by activating PGC‑1α/Nrf2 signaling.

Weiwei Zhi, Kai Li, Hongbing Wang, Ming Lei, Yingqiang Guo

Open access · hybridAbstract read
In one paragraph

Article in International journal of molecular medicine, 2020. 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
1.9field-weighted citation impact, top 16% 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, 17 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

5 authors at 1 institution in 1 country.

Weiwei ZhiDepartment of Cardiology, Xi'an No. 3 Hospital, Xi'an, Shaanxi 710018, P.R. China.
Kai LiDepartment of Cardiology, Xi'an No. 3 Hospital, Xi'an, Shaanxi 710018, P.R. China.
Hongbing WangDepartment of Cardiology, The Affiliated Hospital of Shaanxi University of Chinese Medicine, Xianyang, Shaanxi 712000, P.R. China.
Ming LeiDepartment of Cardiology, Xi'an No. 3 Hospital, Xi'an, Shaanxi 710018, P.R. China.
Yingqiang GuoDepartment of Cardiology, Xi'an No. 3 Hospital, Xi'an, Shaanxi 710018, P.R. China.
Affiliated Hospital of Shaanxi University of Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Melatonin (Mel) elicits beneficial effects on myocardial ischemia/reperfusion injury. However, the underlying mechanism of Mel against oxygen‑glucose deprivation/reperfusion (OGD/R)‑induced H9c2 cardiomyocyte damage remains largely unknown. The aim of the present study was to investigate the biological roles and the potential mechanisms of Mel in OGD/R‑exposed H9c2 cardiomyocytes. The results of the present study demonstrated that Mel significantly elevated the viability and reduced the activity of lactate dehydrogenase and creatine kinase myocardial band in a dose‑ and time‑dependent manner in OGD/R‑insulted H9c2 cells. In addition, Mel suppressed OGD/R‑induced oxidative stress in H9c2 cells, as demonstrated by the decreased reactive oxygen species and malondialdehyde levels, as well as the increased activities of superoxide dismutase, catalase and glutathione peroxidase. Mel exerted an antioxidant effect by activating the peroxisome proliferator‑activated receptor gamma coactivator‑1α (PGC‑1α)/nuclear factor erythroid 2‑related factor 2 (Nrf2) signaling. Mel reduced the expression of OGD/R‑enhanced pro‑inflammatory tumor necrosis factor‑α (TNF‑α), interleukin (IL)‑6, IL‑1β, IL‑8 and monocyte chemotactic protein‑1. Mel also abolished the OGD/R‑induced increase in H9c2 apoptosis, as evidenced by mitochondrial membrane potential restoration and caspase‑3 and caspase‑9 inactivation, as well as the upregulation of Bcl‑2 and downregulation of cleaved caspase‑3 and Bax. The Mel‑induced antiapoptotic effects were dependent on PGC‑1α/TNF‑α signaling. Overall, the results of the present study demonstrated that Mel alleviated OGD/R‑induced H9c2 cell injury via the inhibition of oxidative stress and inflammation by regulating the PGC‑1α/Nrf2 and PGC‑1α/TNF‑α signaling pathways, suggesting a promising role for Mel in the treatment of ischemic heart disease.

Indexed as

AnimalsAntioxidantsApoptosisCell LineGlucoseMelatoninMembrane Potential, MitochondrialMyocardial Reperfusion InjuryMyocytes, CardiacNF-E2-Related Factor 2Oxidative StressOxygenPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaProtective AgentsRatsReactive Oxygen SpeciesAntioxidantsGlucoseMelatoninNfe2l2 protein, ratNF-E2-Related Factor 2OxygenPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPpargc1a protein, ratProtective AgentsReactive Oxygen Species

Identifiers

PMID32323734
PMCPMC7138270
OpenAlexW3007291471

What OpenQuestion holds

Textmetadata
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.