Key result
Piceatannol protects cardiomyocytes from peroxidative injury via PI3K-Akt-eNOS activation and reduced apoptosis.
Why the study?
Few studies have clarified the benefits and cardioprotective mechanisms of piceatannol on cardiomyocytes beyond its anti-oxidative effect.
Does piceatannol pretreatment alleviate acute cardiac injury in H2O2-induced H9c2 cells?
Does piceatannol pretreatment alleviate acute cardiac injury in H2O2-induced H9c2 cells?
Piceatannol protects H9c2 cardiomyocytes from peroxidative injury by upregulating the PI3K-Akt-eNOS signaling pathway.
Piceatannol (3,3′,4,5′-trans-trihydroxystilbene) is a natural polyphenols compound that occurs hydroxylated analogue of resveratrol showing widely biological activities. Previous studies have demonstrated its functions on anti-cancer, neuroprotection and cardioprotection. However, few studies have clarified the benefits of piceatannol on cardiomyocytes except its anti-oxidative effect based on the original property of polyphenols. Here we apply H9c2 cardiomyocytes to study the cardioprotective mechanisms of piceatannol in vitro. We firstly verify its anti-peroxidation effect by using H 2 O 2 -induced in vitro model. Then, flow cytometry results show piceatannol reduce cellular apoptosis by enhancing Bcl-2 expressions in immunoblot analysis. Meantime, piceatannol decreases H 2 O 2 -induced excessive ROS and calcium overloading, and prevents mitochondrial depolarization. Most importantly, piceatannol pretreatment can regulate PI3K-Akt-eNOS signaling pathway to alleviate peroxidative injury. Immunoblot analysis of PI3K, Akt, p-Akt and eNOS shows H 2 O 2 significantly reduces expressions of these proteins. Pretreatment of piceatannol evidently increases their expressions and decreases iNOS expression, implying piceatannol can upregulate PI3K-Akt-eNOS signaling to protect cardiomyocytes from peroxidative injury.
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Wang et al. (2018) studied H2O2-induced acute cardiac injury (in vitro). Piceatannol pretreatment vs. H2O2-induced injury without pretreatment was evaluated on Cellular apoptosis, ROS, calcium overloading, and PI3K-Akt-eNOS signaling protein expressions. Piceatannol pretreatment reduced cellular apoptosis, excessive ROS, and calcium overloading, and upregulated PI3K-Akt-eNOS signaling to protect H9c2 cardiomyocytes from peroxidative injury.
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