期刊
MOLECULAR MEDICINE REPORTS
卷 16, 期 6, 页码 9189-9196出版社
SPANDIDOS PUBL LTD
DOI: 10.3892/mmr.2017.7756
关键词
grape seed proanthocyanidins; hypoxia/reoxygenation; endoplasmic reticulum stress; protein kinase RNA-like ER kinase; H9C2 cardiomyocytes
资金
- First Affiliated Hospital of China Medical University (Shenyang, China)
The aim of the present study was to observe the protective effect of grape seed proanthocyanidins (GSPs) against endoplasmic reticulum (ER) stress-mediated apoptosis caused by hypoxia/ reoxygenation (H/R) injury in H9C2 cardiomyocytes along with its potential mechanisms. H9C2 cardiomyocytes underwent hypoxia for 3 h followed by reoxygenation for 3 h. Different doses of GSPs (50, 100 and 200 mu g/ml) were administered 30 min before hypoxia. Cell viability was assessed, as well as lactic dehydrogenase (LDH) activity, cell apoptosis rate, expression levels of glucose-regulated protein 78 (GRP78), C/EBP-homologous protein (CHOP), protein kinase RNA-like ER kinase (PERK), and eukaryotic translation initiation factor-2 (eIF2 alpha) mRNA and protein. The results revealed that GSPs improved cell viability, reduced LDH activity and reduced the apoptosis rate in cells subjected to H/R, and that the protective effect was most significant when 100 mu g/ml in GSPs was administered. GSPs treatment also decreased mRNA and protein expression of GRP78, CHOP, eIF2 alpha and the level of the phosphorylated form of PERK. Furthermore, GSPs displayed a similar protective effect to that of established ER stress inhibitor 4-phenyl butyric acid. In conclusion, the findings of this study suggest that GSPs may protect H9C2 cardiomyocytes from H/R injury by decreasing ER stress-mediated apoptosis through the suppression of the PERK/eIF2 alpha signaling pathway.
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