07.01.2013 Views

[Abstract Title]. - Society for Neuroscience

[Abstract Title]. - Society for Neuroscience

[Abstract Title]. - Society for Neuroscience

SHOW MORE
SHOW LESS

You also want an ePaper? Increase the reach of your titles

YUMPU automatically turns print PDFs into web optimized ePapers that Google loves.

Aging, LKS Fac. of Med., 4 State Key Lab. of Brain and Cognitive Sci., The Univ. of Hong<br />

Kong, Hong Kong, China<br />

<strong>Abstract</strong>: Oxyresveratrol (OXY) is a natural hydroxylated stilbene existing in mulberry. OXY is<br />

antioxidant, blood-brain-barrier permeable and readily water-soluble. Numerous reports have<br />

shown its neuroprotective effects against Alzheimer‟s disease (AD) and stroke. As little is known<br />

about its neuroprotective effects on Parkinson‟s disease (PD), we investigate whether OXY can<br />

prevent parkinsonian mimetic 6-hydroxydopamine (6-OHDA) neurotoxicity. In SH-SY5Y cells,<br />

both pretreatment and post-treatment with OXY significantly reduced lactate dehydrogenase<br />

release and caspase-3 activity. Moreover, OXY exhibited a wide effective window compared to<br />

resveratrol.<br />

Our experimental results have demonstrated that OXY could penetrate cell membrane by HPLC<br />

analysis of cell extract. In this notion, OXY may act as intracellular antioxidants to significantly<br />

repress the generation of reactive oxygen species (ROS) triggered by 6-OHDA. There<strong>for</strong>e, OXY<br />

markedly attenuated 6-OHDA-induced phosphorylation of JNK and c-Jun. Apart from the<br />

conventional antioxidant activity, we proved that OXY up-regulated the expression of SirT1<br />

repressed by 6-OHDA, and prevented the acetylation of downstream p53.<br />

Taken together, both antioxidant activity and up-regulation of SirT1 by OXY may be responsible<br />

<strong>for</strong> preventing 6-OHDA-induced neurotoxicity, and dietary OXY can be a potential candidate <strong>for</strong><br />

nutritional supplement preventing neurodegeneration from PD.<br />

Disclosures: J.F. Chao, None; M.S. Yu, None; Y.S. Ho, None; M. Wang, None; R.C.C.<br />

Chang, None.<br />

Poster<br />

253. Parkinson's Disease Models: Neuroprotective Mechanisms I<br />

Time: Sunday, November 16, 2008, 1:00 pm - 5:00 pm<br />

Program#/Poster#: 253.5/X6<br />

Topic: C.11.j. Neuroprotective mechanisms: Parkinson‟s disease models<br />

Support: NIH 1R01NS049433-02<br />

<strong>Title</strong>: Tumor necrosis factor-induced p38 MAP kinase activation in dopaminergic<br />

neurodegeneration<br />

Authors: *M. G. TANSEY, L. T. ALTO, I. TREVINO;<br />

Dept Physiol, UT Southwestern Med. Sch. Dallas, Dallas, TX

Hooray! Your file is uploaded and ready to be published.

Saved successfully!

Ooh no, something went wrong!