Research
Ginkgo biloba extract (EGb761) inhibits mitochondria-dependent caspase pathway and prevents apoptosis in hypoxia-reoxygenated cardiomyocytes
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* Corresponding author: Jiangang Shen shenjg@hkucc.hku.hk
1 School of Chinese Medicine, The University of Hong Kong, 10 Sassoon Road, Pokfulam, Hong Kong SAR, China
2 Department of Medicine, The University of Hong Kong, 21 Sassoon Road Pokfulam, Hong Kong SAR, China
3 School of Chinese Medicine, Southern Medical University, Guangzhou 510515, China
Chinese Medicine 2011, 6:8 doi:10.1186/1749-8546-6-8
Published: 23 February 2011Abstract
Background
EGb761 is a standard extract from the leaves of Ginkgo biloba (Yinxing) containing ginkgo-flavone glycosides and terpenoid. The flavonoid components of EGb761 scavenge free radicals and protect myocardia from ischemia-reperfusion injury. The present study aims to determine the effects of the active compounds of EGb761 on mitochondria-dependent caspase pathway.
Methods
Cardiomyocytes were exposed to 24 hours of hypoxia and four hours of reoxygenation, and pretreated with EGb761, bilobalide and quertcetin. By using immunoblot, immunofluorescent, biochemical and flow cytometry techniques, we compared the effects of EGb761 and its representative constituents including quercetin and bilobalides on regulating mitochondria-dependent caspases signal pathway and apoptotic cell death in the hypoxia-reoxygenated cardiomyocytes.
Results
Pretreatment with EGb761 significantly inhibited the release of cytochrome c from mitochondria, the expression of caspase-3, cleavage activities of caspases and attenuated apoptotic cell death. The effects of quercetin on the release of cytochrome c, the cleavage activities of caspases and cell death were similar to those of EGb761 but better than those of bilobalide.
Conclusion
The antioxidant constituents of EGb761 such as quercetin contribute to the cardioprotective effects of EGb761 and inhibit the mitochondria-dependent caspase pathway. It is possible that the mitochondria-dependent caspase pathway may be one of the molecular targets of EGb761 against myocardial ischemia-reperfusion injury.