Abstract
Objectives of the Study
Fisetin (FIS) has a good protective effect on the heart. However, fisetin in regulating the role of the myocardial injury induced by patulin (PAT) is not clear. The aim of this study is to investigate the possible mechanism of fisetin in attenuating patulin induced myocardial injury.
Materials and Methods
Cardiomyocytes were treated with 25μM PAT to set the control group, FIS only group, PAT only group and PAT-FIS addition group. LDH activity, SOD content, and MDA content were evaluated using kits. ROS levels were determined by measuring the intensity of fluorescence. Mitochondrial membrane potential was detected by JC-1 dye staining. The protein expressions of Grp78, Chop and Caspase-12 were detected by Western blot.
Results
In PAT-FIS group, LDH release and MDA content decreased, but SOD content increased. Compared with the control group, the level of ROS in PAT group increased more than 10 times. The level of ROS in the PAT-FIS group was still higher than that in the control group, but it was significantly lower than that in the PAT group. The proportion of red fluorescence in the mitochondrial membrane potential of cardiomyocytes increased from 75% to 85% in the PAT-FIS group. PAT up-regulated the expression of Chop, Grp78 and Caspase-12 proteins, while the overexpression of Chop, Grp78 and Caspase-12 proteins was inhibited after pretreatment with FIS and PAT .
Conclusion
Our findings suggest that FIS inhibits PAT-induced cardiomyocyte apoptosis by regulating ROS/Grp78/Chop/Caspase-12 signaling.