Sulforaphane prevents palmitic acid-induced mitochondrial impairments of cardiomyocyte in vitro

Objective To investigate the protective effect of sulforaphane(SFN)on H9c2 myocardial cells treated with high fat.Methods H9c2 cells were cultured in vitro,and were treated with 350 μmol/L palmitic acid for 24 hours to set up cellinjury model.The model cells were pretreated with different dose of SFN(1,5,7.5,and 10 μmoll/L)for 24 hours and was pretreated by 5 μmol/L SFN for different time(12,24,36,and 48 hours),then the cellular viabilities were detected with trypan blue staining.Fluorescent probes were used to determinate reactive oxygen species(ROS)and mitochondrial membrane potential(MMP).Thiazolyl blue staining was used to detect mitochondrial succinic dehydrogenase(SDH)activity.Mitochondrial morphous was observed with electron microscope.The mRNA expression levels of nuclear respiratory factor 1 and 2(NRF1,NRF2)were detected with reverse transcription polymerase chain reaction(RT-PCR).Results Compared to the control group,the cellular viability of cellinjury model group(38.04±12.69%)decreased(P<0.05),while SFN(5 μmol/L,24 hours)of pretreated group(69.37±6.35%)wase significantly increased(P<0.05).The ROS production of SFN group(86.27±1.44%)was significantly decreased compared to that of cellinjury model group(124.72±11.54 %)(P<0.05).The MMP,SDH activity(37.88±6.92 %,66.59±6.92%)and the mRNA expression levels of NRF1and NRF2(61.72±11.58% and 131.16±14.52%)of SFN group were significantly increased compared to cellinjury model group(P<0.05).SFN pretreatment alleviated mitochondrial pyknosis and mitochondrial quantity reduction.ConclusionSulforaphane can reduce mitochondrial damage induced by high fat,therefore protect myocardial cells exposed to a high-fat environment.