Noscapine protects the H9c2 cardiomyocytes of rats against oxygen-glucose deprivation/reperfusion injury.


Journal

Molecular biology reports
ISSN: 1573-4978
Titre abrégé: Mol Biol Rep
Pays: Netherlands
ID NLM: 0403234

Informations de publication

Date de publication:
Aug 2020
Historique:
received: 16 03 2020
accepted: 23 05 2020
pubmed: 11 7 2020
medline: 23 6 2021
entrez: 11 7 2020
Statut: ppublish

Résumé

Noscapine is an antitumor alkaloid derived from Papaver somniferum plants. Our previous study has demonstrated that exposure of noscapine on primary murine fetal cortical neurons exposed to oxygen-glucose deprivation/reperfusion (OGD/R) has neuroprotective effects. In current study, the effects of noscapine on cardiomyocytes (H9c2 cells) damage caused by 120 minutes (min) of OGD/R were evaluated and we determined whether the addition of BD1047, sigma-one receptor antagonist, prevents the protective effects of noscapine in H9c2 cells through the production of nitric oxide (NO) and apoptosis. To initiate OGD, H9c2 cells was transferred to glucose-free DMEM, and placed in a humidified incubation chamber. Cell viability was assessed with noscapine (1-5 μM) in the presence or absence of BD1047, 24 hours (h) after OGD/R. Cell viability, NO production and apoptosis ratio were evaluated by the MTT assay, the Griess method and the quantitative real-time PCR. Noscapine considerably improved the survival of H9c2 cells compared to OGD/R. Also, noscapine was extremely capable of reducing the concentrations of NO and Bax/Bcl-2 ratio expression. While the BD1047 administration alone diminished cell viability and increased the Bax/Bcl-2 ratio and NO levels. The addition of noscapine in the presence of BD1047 did not increase the cell viability relative to noscapine alone. Noscapine exerted cardioprotective effects exposed to OGD/R-induced injury in H9c2 cells, at least partly via attenuation of NO production and Bax/Bcl-2 ratio, which indicates that the sigma-one receptor activation is involved in the protection by noscapine of H9c2 cells injured by OGD/R.

Identifiants

pubmed: 32648076
doi: 10.1007/s11033-020-05549-6
pii: 10.1007/s11033-020-05549-6
doi:

Substances chimiques

Antitussive Agents 0
Nitric Oxide 31C4KY9ESH
Noscapine 8V32U4AOQU
Glucose IY9XDZ35W2
Oxygen S88TT14065

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

5711-5719

Subventions

Organisme : Iran University of Medical Sciences
ID : IR.IUMS.REC1393.25042

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Auteurs

Gelareh Vahabzadeh (G)

Department of Pharmacology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran. vahabzadeh.g@iums.ac.ir.
Cellular and Molecular Research Center, Iran University of Medical Science, Tehran, Iran. vahabzadeh.g@iums.ac.ir.

Hamidreza Soltani (H)

Department of Pharmacology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.

Mahmood Barati (M)

Department of Biotechnology, Faculty of Allied Medicine, Iran University of Medical Science, Tehran, Iran.

Fereshteh Golab (F)

Cellular and Molecular Research Center, Iran University of Medical Science, Tehran, Iran.

Majid Jafari-Sabet (M)

Department of Pharmacology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.
Razi Drug Research Center, Iran University of Medical Sciences, Tehran, Iran.

Sepideh Safari (S)

Razi Drug Research Center, Iran University of Medical Sciences, Tehran, Iran.

Ashrafolsadat Moazam (A)

Department of Pharmacology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.

Hananeh Mohamadrezaei (H)

Department of Pharmacology and Toxicology, Faculty of Pharmacy and Pharmaceutical Sciences, Tehran Medical Science, Islamic Azad University, Tehran, Iran.

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