Volume 63, Issue 10 pp. 1358-1367

Leaf extract of Rhus verniciflua Stokes protects dopaminergic neuronal cells in a rotenone model of Parkinson's disease

Seung Kim

Corresponding Author

Seung Kim

Department of Alternative Medicine, Gwangju University

These authors contributed equally to this study.

Sung-Jun Kim, Department of Biotechnology, Chosun University, 375 Seosuk-dong, Dong-gu, Gwang-ju, Republic of Korea 501-759.E-mail: [email protected]Search for more papers by this author
Se-Eun Park

Se-Eun Park

Department of Biotechnology, Chosun University, Gwangju

These authors contributed equally to this study.

Search for more papers by this author
Kumar Sapkota

Kumar Sapkota

Department of Biotechnology, Chosun University, Gwangju

Central Department of Zoology, Tribhuvan University, Kirtipur, Kathmandu, Nepal

Search for more papers by this author
Myung-Kon Kim

Myung-Kon Kim

Department of Bio-food Technology, Chonbuk National University, Iksan

Search for more papers by this author
Sung-Jun Kim

Sung-Jun Kim

Department of Biotechnology, Chosun University, Gwangju

Search for more papers by this author
First published: 30 August 2011
Citations: 29

Abstract

Objectives The present study investigated the neuroprotective effects of Rhus verniciflua Stokes (RVS) leaf extract on rotenone-induced apoptosis in human dopaminergic cells, SH-SY5Y.

Methods Cells were pretreated with RVS extract for 1 h then treated with vehicle or rotenone for 24 h. Cell viability, cell cytotoxicity, cell morphology and nuclear morphology were examined by MTT assay, lactate dehydrogenase release assay, phase contrast microscopy and staining with Hoechast 33342, respectively. Reactive oxygen species were measured by 2′7′-dichlorofluorescein diacetate and fragmented DNA was observed by TUNEL assay. Mitochondrial membrane potential was determined by Rhodamine 123. Pro-apoptotic and anti-apoptotic proteins and tyrosine hydroxylase were analysed by Western blotting.

Key findings Results showed that RVS suppressed rotenone-induced reactive oxygen species generation, cellular injury and apoptotic cell death. RVS also prevented rotenone-mediated changes in Bax/Bcl-2 levels, mitochondrial membrane potential dissipation and Caspase 3 activation. Moreover, RVS pretreatment increased the tyrosine hydroxylase levels in SH-SY5Y cells.

Conclusions These findings demonstrate that RVS protects SH-SY5Y cells against rotenone-induced injury and suggest that RVS may have potential therapeutic value for neurodegenerative disease associated with oxidative stress.

The full text of this article hosted at iucr.org is unavailable due to technical difficulties.