Abstract
Bilobalide Protects Pheochromocytoma Cell from Oxygen-Glucose Deprivation/Reperfusion Induced Injury via Activating Wnt1/Beta Catenin Pathway
Department of Neurology, Dongtai People's Hospital, Dongtai, Jiangsu 224200, 1Department of Neurology, Suzhou Clinical Research Center of Neurological Disease, Second Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215004, China
Correspondence Address:
G. Xiao, Department of Neurology, Suzhou Clinical Research Center of Neurological Disease, Second Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215004, China, E-mail: yarrowshaw@hotmail.com
To explore the protective effect of bilobalide on the pheochromocytoma cell injury induced by oxygen-glucose deprivation/reperfusion in vitro. To simulate ischemia-reperfusion condition, the pheochromocytoma cell injury was induced by oxygen-glucose deprivation/reperfusion in vitro. The cells were divided into control, oxygen-glucose deprivation/reperfusion and oxygen-glucose deprivation/ reperfusion+bilobalide groups. The cell viability, proliferative capacity, malondialdehyde level, superoxide dismutase level, apoptosis, Wnt1 protein level and nuclear beta-catenin protein level were assayed. Compared with control group, the cell viability, proliferative capacity, superoxide dismutase level, Wnt1 protein level and nuclear beta-catenin protein level decreased in the oxygen-glucose deprivation/ reperfusion group, malondialdehyde level and the percentage of apoptotic cells increased in the oxygenglucose deprivation/reperfusion group, while the cells were treated with bilobalide in the oxygen-glucose deprivation/reperfusion+bilobalide group, all the above-mentioned observation indicators recovered to a certain extent, but still did not reach the level of the control group. Bilobalide protects pheochromocytoma cell from oxygen-glucose deprivation/reperfusion induced injury in vitro through inhibiting oxidative stress via activating Wnt1/beta-catenin pathway.
