Abstract
Ischemic cerebrovascular disease is a global health problem. According to the World Health Organization, ischemic stroke is actually the most common cause of death in the world. Ginkgo biloba extract (GbE) is a traditional Chinese medicine for angina pectoris. Ginkgo biloba plays a role in expanding blood vessels, increasing coronary and cerebral blood flow, preventing platelet aggregation, inhibiting thrombosis, and improving the microcirculation. In the present study, we investigated the mechanisms involved in the neuroprotective effects of GbE in a model of hypoxic-ischemic brain disease. We used NGF(100 ng/ml for 6 days)and OGD(5% CO2and 95% N2, 1 mmol/l NaS2O4insugar-free DMEM for 16 h) to stimulate PC12 cells and convert them into neurons in order to establish an ischemia model. The results showed that PC12 cells transformed into cells that looked like neurons and that MAP2 was up-regulated in NGF-treated PC12 cells. Cell apoptosis was found to be up-regulated after NGF stimulation and OGD. The apoptosis rate after 16 hours of OGD was 19.44%. GbE (50ng/ml) reduces apoptosis rate to 11.35%. These results may help to show that NGF treatment can be combined with OGD to establish anin vitromodel of acute ischemic brain damage. In the present study, we find that GbE effectively increases the survival rate of PC12 cells and relieves OGD damage. These results suggest that GbE has the neuroprotective effects of ischemic brain damage.
Highlights
Ischemic stroke occurs when the blood supply to the brain is obstructed
OGD is a model of oxygen and glucose shortage
We used NGF combined with OGD to set up an ischemia tolerance model
Summary
Ischemic stroke occurs when the blood supply to the brain is obstructed. Effective methods of preventing and controlling ischemic cerebrovascular disease have been a topic of great interest. The GbE displays, mainly via its flavonoid constituents, free radical scavenging and antioxidant actions that are probably associated with its protective actions in animal models of hypoxia and ischaemia [2]. Studies support the potential usefulness of GbE in AD and in vascular dementia. The oxygen-glucose deprivation of PC12 cells was used to establish a cerebral hypoxia-ischemia model to investigate the mechanism of GbE neuroprotection. We measure the induction of superoxide dismutase (SOD) in an attempt to elucidate possible mechanisms that underlie GbE-mediated protection against OGD in PC12 cells
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