title: Neuroprotection against cobalt chloride-induced cell apoptosis of primary cultured cortical neurons by salidroside.
abstract: Salidroside, a phenol glycoside of plant origin, has been documented to possess a broad spectrum of pharmacological properties, including protective effects against neuronal death induced by different insults. To provide further insights into the neuroprotective functions peculiar to salidroside, this study used primary cultured cortical neurons of rats as a cell model to examine whether salidroside was able to prevent against cell damage after exposure to cobalt chloride (CoCl(2)), a hypoxia-inducing agent. The data from 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide test, Hoechst33342 staining, terminal deoxynucleotidyl transferase dUTP-mediated nicked end labeling assay, and Bax/Bcl-2 ratio analysis indicated that salidroside pretreatment attenuated hypoxia-induced apoptotic cell death of primary cultured cortical neurons in a dose-dependent manner. Moreover, preliminary exploration of the possible mechanisms suggested that the protective effects of salidroside, shown in our experimental setting, might probably be mediated by enhancing the expression of hypoxia-inducible factor-1α, alleviating the increase of intracellular reactive oxygen species levels, and inhibiting over-expression of nuclear factor-kappa B protein.
authors.affiliation: Jiangsu Key Laboratory of Neuroregeneration, Nantong University, 19 Qixiu Road, Nantong 226001, Jiangsu, People's Republic of China.
authors.forename: Shuqiang
authors.initials: S
authors.lastname: Zhang
authors.forename: Xia
authors.initials: X
authors.lastname: Chen
authors.forename: Yumin
authors.initials: Y
authors.lastname: Yang
authors.forename: Xinyang
authors.initials: X
authors.lastname: Zhou
authors.forename: Jie
authors.initials: J
authors.lastname: Liu
authors.forename: Fei
authors.initials: F
authors.lastname: Ding
mesh_terms: D000818:Animals; D017209:Apoptosis; D018929:Cell Culture Techniques; D002467:Cell Nucleus / Q000187:drug effects / Q000378:metabolism; D002470:Cell Survival; D002478:Cells, Cultured; D002540:Cerebral Cortex / Q000166:cytology* / Q000196:embryology; D003035:Cobalt; D004353:Drug Evaluation, Preclinical; D005960:Glucosides / Q000494:pharmacology*; D051795:Hypoxia-Inducible Factor 1, alpha Subunit / Q000378:metabolism; D016328:NF-kappa B / Q000378:metabolism; D009474:Neurons / Q000187:drug effects* / Q000502:physiology; D018696:Neuroprotective Agents / Q000494:pharmacology*; D010636:Phenols / Q000494:pharmacology*; D021381:Protein Transport; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D051381:Rats; D017382:Reactive Oxygen Species / Q000378:metabolism; D051028:bcl-2-Associated X Protein / Q000378:metabolism
chemical_list: D005960:Glucosides; C497444:Hif1a protein, rat; D051795:Hypoxia-Inducible Factor 1, alpha Subunit; D016328:NF-kappa B; D018696:Neuroprotective Agents; D010636:Phenols; D019253:Proto-Oncogene Proteins c-bcl-2; D017382:Reactive Oxygen Species; D051028:bcl-2-Associated X Protein; D003035:Cobalt; C018021:cobaltous chloride; C009172:rhodioloside