TY - JOUR AU - LI Yun-peng AU - WANG Shu-lin AU - LIU Bei AU - TANG Lu AU - KUANG Rong-ren AU - WANG Xian-bao AU - ZHAO Cong AU - SONG Xu-dong AU - CAO Xue-ming AU - WU Xiang AU - YANG Ping-zhen AU - WANG Li-zi AU - CHEN Ai-hua PY - 2017 TI - Sulforaphane prevents rat cardiomyocytes from hypoxia/reoxygenation injury in vitro via activating SIRT1 and subsequently inhibiting ER stress JF - Acta Pharmacologica Sinica; Vol 37, No 3 (March 2016): Acta Pharmacologica Sinica Y2 - 2017 KW - N2 - Aim: 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 . Methods: 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. Results: 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. Conclusion: SFN prevents cardiomyocytes from H/R injury in vitro most likely via activating SIRT1 pathway and subsequently inhibiting the ER stress-dependent apoptosis. UR - http://www.chinaphar.com/article/view/9442