Ginkgetin, the extract of Ginkgo biloba leaves, has been reported to exert preventive and
therapeutic effects on
cardiovascular disease. However, little is known about its role in
myocardial ischemia-
reperfusion injury (MIRI). The present study aimed to unveil the function of
ginkgetin in cardiomyocytes subjected to
hypoxia/reoxygenation (H/R) injury. Cell Counting Kit-8 (CCK-8) was employed to evaluate the impact of
ginkgetin on cell viability in the absence or presence of H/R. Proinflammatory
cytokines and
malondialdehyde (MDA),
reactive oxygen species (SOD), and
lactate dehydrogenase (LDH) were determined via corresponding kits. In addition, flow cytometry was performed to detect apoptotic level. Western blot analysis was utilized to estimate
caspase-3 and
cytochrome C.
Ginkgetin had no significant effect on cell viability; however, it could enhance viability of H9C2 cells exposed to H/R.
Inflammation and oxidative stress induced by H/R injury were relieved via pretreatment with
ginkgetin. Preconditioning of
ginkgetin also decreased apoptotic rate and the
protein levels of
caspase-3,
cytochrome C under H/R condition. Furthermore, 2-HBA, an inducer of
caspase-3, was used for the activation of
caspase-3 signaling pathway. It was found that induction of
caspase-3 eliminated the protective effect of
ginkgetin on H9C2 cells exposed to H/R. These results indicated that
ginkgetin attenuated
inflammation, oxidative stress, and apoptosis. These protective roles of
ginkgetin may attribute to
caspase-3 dependent pathway.