ArticleMolecular biology reports2017
Ghrelin protected neonatal rat cardiomyocyte against hypoxia/reoxygenation injury by inhibiting apoptosis through Akt-mTOR signal.
Article in Molecular biology reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 18 citations in OpenAlex.
- Emerging Relevance of Ghrelin in Programmed Cell Death and Its Application in Diseases.International journal of molecular sciences · 2023Review
- Article
- Ghrelin Relieves Obesity-Induced Myocardial Injury by Regulating the Epigenetic Suppression of miR-196b Mediated by lncRNA HOTAIR.Obesity facts · 2022Article
- Research progress of ghrelin on cardiovascular disease.Bioscience reports · 2021Review
- Protective Effect of a Novel Polysaccharide fromBioMed research international · 2020Article
- Snapshot: Implications for mTOR in Aging-related Ischemia/Reperfusion Injury.Aging and disease · 2019Review
- Hongjingtian Injection Attenuates Myocardial Oxidative Damage via Promoting Autophagy and Inhibiting Apoptosis.Oxidative medicine and cellular longevity · 2017Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Reducing reperfusion period myocardial cell damage is efficient to reduce myocardial ischemia-reperfusion injury. Ghrelin can increase myocardial contractility, improve heart failure caused by myocardial infarction. This study aimed to investigate the protective effect of Ghrelin on myocardial hypoxia/reoxygenation (H/R) injury of neonatal rat cardiomyocytes (NRCMs) and to explore the mechanisms. We isolated the NRCMs, established myocardial H/R model, blocked growth hormone secretagogue receptor (GHSR) by siRNA technique, examined cell activity by MTT and LDH assay, detected apoptosis by Hoechst 33258 staining and flow cytometry and determined the expression levels of apoptosis related proteins and signaling pathway proteins by western blot. We found that Ghrelin can significantly improve cell activity and decrease apoptosis after H/R, however this effect was abolished by GHSR-siRNA. In addition, we found that Ghrelin can significantly increase the expression of Bcl-2 but inhibit the level of Bax and caspase-3. Further mechanism study found that the phosphorylation level of signaling pathway protein Akt and mTOR in Ghrelin treated group were significantly higher than that in other groups. In conclusion, Ghrelin can reduce the H/R damage on NRCMs and inhibit the apoptosis by activating Akt-mTOR signaling pathway.
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