Can we predict who is at risk of facing cognitive issues in PD and address them earlier? These are the questions being pursued by Dr. Goldman of the PDF Research Center at Rush University Medical Center.
PDF Grant Programs
Are you interested in furthering Parkinson's science? View PDF's open grant programs.
Involvement of activation of the Nrf2/ARE pathway in protection against 6-OHDA-induced SH-SY5Y cell death by ?-iso-cubebenol.
PDF's targeted PubMed search provides you with access to journal articles from the last 90 days that may be pertinent to Parkinson's disease research.
Not what you're looking for? Do you need informational publications about Parkinson's targeted for people living with Parkinson's, caregivers and family members? Please browse PDF's educational materials and programs - which are all available electronically or in print. Order for yourself, a loved one or in bulk for your patients or support group.
Neurotoxicology 2014 Jul; 44C:160-168
Authors: Sun Young Park, Do Yeon Kim, Jong-Koo Kang, Geuntae Park, Young-Whan Choi
Free radical-mediated neurodegeneration is one of the many causes of Parkinson's disease (PD). As part of our ongoing studies on the identification of biologically active Schisandra chinensis components, we have isolated and structurally elucidated ?-iso-cubebenol. This study was carried out in an attempt to clarify the neuroprotective effect of ?-iso-cubebenol on toxin-insulted dopaminergic neuronal death using 6-hydroxy-dopamine (6-OHDA)-induced dopaminergic SH-SY5Y cells. ?-iso-cubebenol significantly attenuated the loss of mitochondrial function (MTT assay) and membrane integrity (lactate dehydrogenase assay) associated with 6-OHDA-induced neurotoxicity. Pretreatment of the cells with ?-iso-cubebenol diminished the intracellular accumulation of reactive oxygen species (ROS) and calcium in response to 6-OHDA. Moreover, ?-iso-cubebenol protected against 6-OHDA-induced neurotoxicity through inhibition of SH-SY5Y cell apoptosis. In addition, JC-1 staining, which is a well-established measure of mitochondrial damage, was decreased after treatment with ?-iso-cubebenol. Notably, ?-iso-cubebenol inhibited the release of mitochondrial flavoprotein apoptosis inducing factor (AIF) from the mitochondria to the cytosol and nucleus following 6-OHDA treatment. In addition, ?-iso-cubebenol reduced the 6-OHDA-induced phosphorylation of ERK and induced the phosphorylation of PKA, PKB, and CREB in a dose-dependent manner. Moreover, ?-iso-cubebenol stimulated the activation of Nrf2, a downstream target of CREB. Furthermore, ?-iso-cubebenol stimulated the expression of multiple antioxidant response genes (NQO-1 and HO-1). Finally, CREB and Nrf2 siRNA transfection diminished ?-iso-cubebenol-mediated neuroprotection.
PMID: 24997245 [PubMed - as supplied by publisher]