Hyperoside protects against hypoxia/reoxygenation induced injury in cardiomyocytes by suppressing the Bnip3 expression.

Abstract

AIMS:

Role of hyperoside in protecting cardiomyocytes from ischemia/reperfusion induced injury has been proved. However, possible protecting mechanisms remain unclear. To fix the problem, an essential pro-apoptotic protein Bnip3 was studied in our experiments.

METHODS AND RESULTS:

Neonatal rat cardiomyocytes were used and submitted to hypoxia for 8h followed by reoxygenation for 2h to simulate the ischemia/reperfusion injury. Hypoxia/reoxygenation(H/R) induced damage to cardiomyocytes and the protective effect of hyperoside were examined by means of MTT assay. H/R-induced apoptosis was assessed by Terminal-deoxynucleoitidyl Transferase Mediated Nick End Labeling(TUNEL) and DNA Ladder assay. mRNA expression of Bnip3 was determined by use of quantitative real-time reverse transcription polymerase chain reaction assay. Protein levels of Bnip3, Bax, Bcl-2 and cleaved caspase-3 were examined using western-blot assay. Our results showed that H/R caused great damage to cardiomyocytes, upregulated the protein expressions of Bnip3, Bax, cleaved caspase3, and decreased the expression of the anti-apoptotic protein of Bcl-2. Whereas, compared with the H/R group, a decrease in activities of Bnip3, Bax, cleaved caspase3, and a promoting expression of Bcl-2 were detected in the H/R goup pretreated with hyperoside.

CONCLUSION:

It was concluded in our study that H/R-induced apoptotic effect in cardiomyocytes could be attenuated by hyperoside, and the protective role of hyperoside, if not completely, could be partly through the suppression of the pro-apoptotic gene Bnip3.

• Authors: Rui Xiao, An-Li Xiang, Hong-Bo Pang, Ke-Qiang Liu
• Journal: Gene (Gene) Vol. 629 Pg. 86-91 (Sep 20 2017) ISSN: 1879-0038 [Electronic] Netherlands
• PMID: 28754633 (Publication Type: Journal Article)
• Copyright: Copyright © 2017 Elsevier B.V. All rights reserved.

Chemical References

• BNIP3 protein, rat
• Cardiotonic Agents
• Membrane Proteins
• Mitochondrial Proteins
• hyperoside
• Quercetin

Topics

• Animals
• Apoptosis
• Cardiotonic Agents (pharmacology)
• Membrane Proteins (genetics, metabolism)
• Mitochondrial Proteins (genetics, metabolism)
• Myocardial Infarction (metabolism, pathology)
• Myocytes, Cardiac (drug effects, metabolism, pathology)
• Plants, Medicinal (chemistry)
• Quercetin (analogs & derivatives, pharmacology)
• Rats
• Rats, Sprague-Dawley
• Reperfusion Injury (metabolism, pathology)