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The present study aimed to investigate the protective effects of salidroside (SAL) on 1‐methyl‐4‐phenylpyridinium (MPP+)‐induced PC12 cell model for Parkinson's disease. PC12 cells were pretreated with SAL in different concentrations and then exposed to MPP+. To evaluate the effects of SAL on cytotoxicity, the survival rate was tested by the 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐dimethyltetrazolium bromide (MTT) assay and the apoptosis was tested via flow cytometry and Western blot. Reactive oxygen species (ROS), glutathione (GSH), and malondialdehyde (MDA) were detected to analyze the effects of SAL on oxidative stress. The mRNA and protein levels of inflammatory factors TNF‐α and IL‐1β were also determined by real‐time quantitative polymerase chain reaction and Western blot. Pretreatment with SAL effectively relieved the MPP+ cytotoxic effects and decreased the release of ROS production and inflammatory cytokines. SAL also inhibited apoptosis, suppressed MDA activity, and increased GSH levels in MPP+‐treated PC12 cells. Moreover, the expression levels of caspase‐9, caspase‐3, and Bax were significantly decreased in the SAL treatment groups compared with the MPP+ group, whereas Bcl‐2 expression was significantly increased in the SAL treatment groups. In summary, the overall results suggested that SAL have neuroprotective effects on the MPP+‐induced PC12 cell model by inhibiting inflammation, oxidative stress, and cell apoptosis. SAL may be a potential active product to protect against Parkinson's disease. [ABSTRACT FROM AUTHOR]

The present study aimed to investigate the protective effects of salidroside (SAL) on 1-methyl-4-phenylpyridinium (MPP + )-induced PC12 cell model for Parkinson's disease. PC12 cells were pretreated with SAL in different concentrations and then exposed to MPP + . To evaluate the effects of SAL on cytotoxicity, the survival rate was tested by the 3-(4,5-dimethylthiazol-2-yl)-2,5-dimethyltetrazolium bromide (MTT) assay and the apoptosis was tested via flow cytometry and Western blot. Reactive oxygen species (ROS), glutathione (GSH), and malondialdehyde (MDA) were detected to analyze the effects of SAL on oxidative stress. The mRNA and protein levels of inflammatory factors TNF-α and IL-1β were also determined by real-time quantitative polymerase chain reaction and Western blot. Pretreatment with SAL effectively relieved the MPP + cytotoxic effects and decreased the release of ROS production and inflammatory cytokines. SAL also inhibited apoptosis, suppressed MDA activity, and increased GSH levels in MPP + -treated PC12 cells. Moreover, the expression levels of caspase-9, caspase-3, and Bax were significantly decreased in the SAL treatment groups compared with the MPP + group, whereas Bcl-2 expression was significantly increased in the SAL treatment groups. In summary, the overall results suggested that SAL have neuroprotective effects on the MPP + -induced PC12 cell model by inhibiting inflammation, oxidative stress, and cell apoptosis. SAL may be a potential active product to protect against Parkinson's disease., (© 2018 International Union of Biochemistry and Molecular Biology, Inc.)