Sulforaphane prevents rat cardiomyocytes from hypoxia/reoxygenation injury in vitro via activating SIRT1 and subsequently inhibiting ER stress
العنوان: | Sulforaphane prevents rat cardiomyocytes from hypoxia/reoxygenation injury in vitro via activating SIRT1 and subsequently inhibiting ER stress |
---|---|
المؤلفون: | Xueming Cao, Xudong Song, Xiang Wu, Rong-ren Kuang, Xianbao Wang, Shulin Wang, Bei Liu, Lu Tang, Pingzhen Yang, Yunpeng Li, Cong Zhao, Lizi Wang, Aihua Chen |
المصدر: | Acta Pharmacologica Sinica. 37:344-353 |
بيانات النشر: | Springer Science and Business Media LLC, 2016. |
سنة النشر: | 2016 |
مصطلحات موضوعية: | 0301 basic medicine, Cardiotonic Agents, Cell Survival, Apoptosis, Myocardial Reperfusion Injury, Rats, Sprague-Dawley, 03 medical and health sciences, chemistry.chemical_compound, 0302 clinical medicine, Sirtuin 1, Isothiocyanates, medicine, Animals, Myocyte, Myocytes, Cardiac, Pharmacology (medical), Cells, Cultured, Membrane Potential, Mitochondrial, Pharmacology, Traditional medicine, biology, business.industry, General Medicine, Hypoxia (medical), Endoplasmic Reticulum Stress, Cell Hypoxia, In vitro, Rats, Cell biology, 030104 developmental biology, chemistry, Sulfoxides, 030220 oncology & carcinogenesis, Unfolded protein response, biology.protein, Original Article, Signal transduction, medicine.symptom, business, hormones, hormone substitutes, and hormone antagonists, Signal Transduction, Sulforaphane |
الوصف: | Sulforaphane (SFN), a natural dietary isothiocyanate, is found to exert beneficial effects for cardiovascular diseases. This study aimed to investigate the mechanisms underlying the protective effects of SFN in a model of myocardial hypoxia/reoxygenation (H/R) injury in vitro.Cultured neonatal rat cardiomyocytes pretreated with SFN were subjected to 3-h hypoxia followed by 3-h reoxygenation. Cell viability and apoptosis were detected. Caspase-3 activity and mitochondrial membrane potential (ΔΨm) was measured. The expression of ER stress-related apoptotic proteins were analyzed with Western blot analyses. Silent information regulator 1 (SIRT1) activity was determined with SIRT1 deacetylase fluorometric assay kit.SFN (0.1-5 μmol/L) dose-dependently improved the viability of cardiomyocytes, diminished apoptotic cells and suppressed caspase-3 activity. Meanwhile, SFN significantly alleviated the damage of ΔΨm and decreased the expression of ER stress-related apoptosis proteins (GRP78, CHOP and caspase-12), elevating the expression of SIRT1 and Bcl-2/Bax ratio in the cardiomyocytes. Co-treatment of the cardiomyocytes with the SIRT1-specific inhibitor Ex-527 (1 μmol/L) blocked the SFN-induced cardioprotective effects.SFN prevents cardiomyocytes from H/R injury in vitro most likely via activating SIRT1 pathway and subsequently inhibiting the ER stress-dependent apoptosis. |
تدمد: | 1745-7254 1671-4083 |
الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::2b0670f1c96494abf9867d8e6237b18dTest https://doi.org/10.1038/aps.2015.130Test |
حقوق: | OPEN |
رقم الانضمام: | edsair.doi.dedup.....2b0670f1c96494abf9867d8e6237b18d |
قاعدة البيانات: | OpenAIRE |
تدمد: | 17457254 16714083 |
---|