title: Salvianolic acid B protects SH-SY5Y neuroblastoma cells from 1-methyl-4-phenylpyridinium-induced apoptosis.
abstract: Parkinson's disease (PD) is associated with mitochondrial dysfunction, oxidative stress, and activation of the apoptotic cascade. In the study, we investigated the effects of salvianolic acid B (Sal B) on 1-methyl-4-phenylpyridinium (MPP(+))-treated SH-SY5Y cells, a classic in vitro model for PD. We found Sal B inhibited the loss of cell viability by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The underlying mechanisms of Sal B action were further studied. Treatment of SH-SY5Y cells with MPP(+) caused a loss of cell viability and mitochondrial membrane potential, condensation of nuclei, elevation in the level of reactive oxygen species (which was associated with cytochrome c release), an increase in the Bax/Bcl-2 mRNA ratio, and activation of caspase-3. Sal B ameliorated the MPP(+)-altered phenotypes. These results indicate that the Sal B protected SH-SY5Y cells against MPP(+)-induced apoptosis by relieving oxidative stress and modulating the apoptotic process. Our findings suggest that salvianolic acid B may be a promising agent to prevent PD.
authors.affiliation: Institute of Integrative Medicine, Xiangya Hospital, Central South University, Changsha 410008, P. R. China.
authors.forename: Guang
authors.initials: G
authors.lastname: Zeng
authors.forename: Tao
authors.initials: T
authors.lastname: Tang
authors.forename: Han-Jun
authors.initials: HJ
authors.lastname: Wu
authors.forename: Wan-Hui
authors.initials: WH
authors.lastname: You
authors.forename: Jie-Kun
authors.initials: JK
authors.lastname: Luo
authors.forename: Yuan
authors.initials: Y
authors.lastname: Lin
authors.forename: Qing-Hua
authors.initials: QH
authors.lastname: Liang
authors.forename: Xing-Qun
authors.initials: XQ
authors.lastname: Li
authors.forename: Xi
authors.initials: X
authors.lastname: Huang
authors.forename: Qi-Dong
authors.initials: QD
authors.lastname: Yang
mesh_terms: D015655:1-Methyl-4-phenylpyridinium / Q000633:toxicity*; D000978:Antiparkinson Agents / Q000737:chemistry / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects*; D001572:Benzofurans / Q000737:chemistry / Q000494:pharmacology*; D001681:Biological Assay; D053148:Caspase 3 / Q000096:biosynthesis; D018929:Cell Culture Techniques; D045744:Cell Line, Tumor; D002470:Cell Survival / Q000187:drug effects; D006801:Humans; D053078:Membrane Potential, Mitochondrial / Q000187:drug effects; D015394:Molecular Structure; D009447:Neuroblastoma; D010300:Parkinson Disease / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control; D051560:Proto-Oncogene Proteins c-bcl-6 / Q000096:biosynthesis; D017382:Reactive Oxygen Species / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D051028:bcl-2-Associated X Protein / Q000096:biosynthesis; D053630:Depsides
chemical_list: D015655:1-Methyl-4-phenylpyridinium; D000978:Antiparkinson Agents; D001572:Benzofurans; D053148:Caspase 3; D051560:Proto-Oncogene Proteins c-bcl-6; D017382:Reactive Oxygen Species; D051028:bcl-2-Associated X Protein; C494826:BAX protein, human; C076944:salvianolic acid B; D053630:Depsides