title: Baicalein attenuates 6-hydroxydopamine-induced neurotoxicity in SH-SY5Y cells.
abstract: It has been suggested that baicalein, a flavonoid obtained from the Scutellaria root, exerts a protective role on neurons against several neuronal insults. However, the protective mechanisms underlying this protective effect remain largely unknown. Our results indicate that baicalein protects SH-SY5Y cells, a dopaminergic neuronal cell line, from 6-hydroxydopamine (6-OHDA)-induced damage by the attenuation of reactive oxygen species (ROS). In order to determine the effects of baicalein on mitochondrial events, mitochondrial membrane potentials (deltapsim) and caspase cascades downstream of mitochondria were assessed. Baicalein inhibited the collapse of deltapsim, suggesting that baicalein reduces the mitochondrial dysfunction associated with 6-OHDA treatment. Baicalein also inhibited caspase-9 and caspase-3 activation, which can be triggered by mitochondrial malfunctions. Furthermore, baicalein induced a significant reduction in the level of phospho-JNK, which is known as an apoptotic mediator in 6-OHDA-induced neuronal cell death. Our results indicate that baicalein protects neurons from the deleterious effects of 6-OHDA via the attenuation of oxidative stress, mitochondrial dysfunction, caspase activity, and JNK activation.
authors.affiliation: Department of Anatomy and Cell Biology, College of Medicine, Chung Ang University, Dongjak-ku, Seoul, Republic of Korea.
authors.forename: Hyun Jung
authors.initials: HJ
authors.lastname: Lee
authors.forename: Yoo Hun
authors.initials: YH
authors.lastname: Noh
authors.forename: Do Yeon
authors.initials: DY
authors.lastname: Lee
authors.forename: Yong Sik
authors.initials: YS
authors.lastname: Kim
authors.forename: Kyung Yong
authors.initials: KY
authors.lastname: Kim
authors.forename: Yoon Hee
authors.initials: YH
authors.lastname: Chung
authors.forename: Won Bok
authors.initials: WB
authors.lastname: Lee
authors.forename: Sung Su
authors.initials: SS
authors.lastname: Kim
mesh_terms: D017209:Apoptosis / Q000187:drug effects; D061945:Caspase Inhibitors; D020169:Caspases / Q000032:analysis; D045744:Cell Line, Tumor; D002470:Cell Survival / Q000187:drug effects; D004789:Enzyme Activation / Q000187:drug effects; D044950:Flavanones / Q000737:chemistry / Q000494:pharmacology*; D006801:Humans; D048031:JNK Mitogen-Activated Protein Kinases / Q000378:metabolism; D008564:Membrane Potentials / Q000187:drug effects; D008928:Mitochondria / Q000187:drug effects; D008954:Models, Biological; D015394:Molecular Structure; D009447:Neuroblastoma / Q000473:pathology; D009474:Neurons / Q000187:drug effects* / Q000473:pathology; D018696:Neuroprotective Agents / Q000378:metabolism / Q000494:pharmacology*; D018384:Oxidative Stress / Q000187:drug effects; D016627:Oxidopamine / Q000378:metabolism / Q000633:toxicity*; D010300:Parkinson Disease / Q000188:drug therapy / Q000378:metabolism; D013565:Sympatholytics / Q000378:metabolism / Q000633:toxicity*; D013997:Time Factors
chemical_list: D061945:Caspase Inhibitors; D044950:Flavanones; D018696:Neuroprotective Agents; D013565:Sympatholytics; C006680:baicalein; D016627:Oxidopamine; D048031:JNK Mitogen-Activated Protein Kinases; D020169:Caspases