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 tradit...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.展开更多
文摘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.
