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      Effect of Oleracein E, a Neuroprotective Tetrahydroisoquinoline, on Rotenone-Induced Parkinson’s Disease Cell and Animal Models

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          Abstract

          Oleracein E (OE), a tetrahydroisoquinoline possessing potent antioxidant activity, was first isolated from a traditional Chinese medicine, Portulaca oleraea L., and is hypothesized to be a neuroprotectant. In the present study, we evaluated the effects of racemic OE on rotenone-induced toxicity in Parkinson's disease (PD) cell and animal models. Pretreatment with OE (10 μM, 2 h) decreased lactic acid dehydrogenase (LDH) release and the apoptosis rate in rotenone (5 μM, 24 h)-treated SH-SY5Y human neuroblastoma cells. Further mechanistic study indicated that OE reduced reactive oxygen species (ROS) levels, inhibited extracellular signal-regulated kinase (ERK) 1/2 phosphorylation, reduced rotenone-induced up-regulation of the proapoptotic protein Bax, and prevented cytochrome C release and caspase-3 activation. In a rotenone-treated (intragastric 30 mg/(kg·d), 56 d) C57BL-6J mouse model, OE (intragastric 15 mg/(kg·d), 56 d) improved motor function, as indicated by an increased moving distance in the spontaneous activity test and sustained time on the rota-rod test. OE also elevated superoxide dismutase (SOD) activity, decreased malonaldehyde content, and reduced ERK1/2 phosphorylation in the midbrain and striatum of mice treated with rotenone. Furthermore, OE preserved tyrosine hydroxylase-positive neurons and maintained the density of dopaminergic (DAergic) fibers in the substantia nigra pars compacta (SNpc). Some of the effects of OE on PD models were similar to those of the positive control selegiline hydrochloride. Our results demonstrated that OE protects DAergic neurons against rotenone toxicity through reducing oxidative stress and down-regulating stress-related molecules. OE is worth exploring further for its neuroprotectant properties in the prevention and treatment of PD.

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          Author and article information

          Journal
          ACS Chemical Neuroscience
          ACS Chem. Neurosci.
          American Chemical Society (ACS)
          1948-7193
          1948-7193
          October 10 2016
          January 18 2017
          October 25 2016
          January 18 2017
          : 8
          : 1
          : 155-164
          Affiliations
          [1 ]School of Pharmaceutical Sciences, Shandong University, Jinan 250012, China
          [2 ]School of Basic Medical Sciences, Shandong University, Jinan 250012, China
          [3 ]Jinan Hongjitang Pharmaceutical Co. Ltd., Jinan 250100, China
          Article
          10.1021/acschemneuro.6b00291
          27731637
          d2d581f3-76c9-4345-8698-7733d4957133
          © 2017
          History

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