title: Protective Effect of Puerarin Against Oxidative Stress Injury of Neural Cells and Related Mechanisms.
abstract: BACKGROUND Parkinson's disease (PD) is manifested as degeneration of dopaminergic neurons in substantia nigra compacta. The mitochondrial dysfunction induced by oxidative stress is believed to a major cause of PD. Puerarin has been widely applied due to its estrogen nature and anti-oxidative function. This study thus investigated the protective role of puerarin against oxidative stress injury on PC12 neural cells, in addition to related mechanisms. MATERIAL AND METHODS PC12 cells were pre-treated with gradient concentrations of puerarin, followed by the induction of 0.5 mM H2O2. MTT assay was used to detect cell viability. Enzyme-linked immunosorbent assay (ELISA) was employed to detect intracellular level of superoxide dismutase (SOD), malondialdehyde (MDA), and glutathione (GSH). Cell apoptosis was determined by Annexin-V/7-AAD double labelling. Reactive oxidative species (ROS) and lactate dehydrogenase (LDH) activities were then measured. Cellular levels of caspase-3 and caspase-9 were also determined. RESULTS The pre-treatment using puerarin significantly reversed H2O2-induced oxidative stress injury, as it can increase proliferation, SOD and GSH activities, decrease MDA activity, suppress apoptosis of PC12 cells, and decrease ROS and LDH production (p<0.05 in all cases). Further assays showed depressed up-regulation of caspase-3 and caspase-9 after puerarin pretreatment. CONCLUSIONS Puerarin pretreatment can decrease activity of caspase-3 and caspase-9 activity in PC12 cells, thus protecting cells from oxidative injury.
authors.affiliation: Department of Neurology, The Affiliated Hospital to Changchun University of Chinese Medicine, Changchun, Jilin, China (mainland).
authors.forename: Yuan
authors.initials: Y
authors.lastname: Cheng
authors.affiliation: Department of Neurology, The Affiliated Hospital to Changchun University of Chinese Medicine, Changchun, Jilin, China (mainland).
authors.forename: Wei
authors.initials: W
authors.lastname: Leng
authors.affiliation: Department of Neurology, The Affiliated Hospital to Changchun University of Chinese Medicine, Changchun, Jilin, China (mainland).
authors.forename: Jingshu
authors.initials: J
authors.lastname: Zhang
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology; D017209:Apoptosis / Q000187:drug effects; D053148:Caspase 3 / Q000378:metabolism; D053453:Caspase 9 / Q000378:metabolism; D002470:Cell Survival / Q000187:drug effects; D002478:Cells, Cultured; D005978:Glutathione / Q000378:metabolism; D007529:Isoflavones / Q000494:pharmacology*; D008315:Malondialdehyde / Q000378:metabolism; D009474:Neurons / Q000187:drug effects* / Q000378:metabolism* / Q000473:pathology; D018696:Neuroprotective Agents / Q000494:pharmacology; D018384:Oxidative Stress / Q000187:drug effects*; D016716:PC12 Cells; D051381:Rats; D017382:Reactive Oxygen Species / Q000378:metabolism; D013482:Superoxide Dismutase / Q000378:metabolism
chemical_list: D000975:Antioxidants; D007529:Isoflavones; D018696:Neuroprotective Agents; D017382:Reactive Oxygen Species; D008315:Malondialdehyde; D013482:Superoxide Dismutase; D053148:Caspase 3; D053453:Caspase 9; D005978:Glutathione; C033607:puerarin