alexa Abstract | Neurotoxic effect of salsolinol through oxidative stress induction and Nrf2-Keap1 signalling regulation

Journal of Chemical and Pharmaceutical Research
Open Access

OMICS International organises 3000+ Global Conferenceseries Events every year across USA, Europe & Asia with support from 1000 more scientific Societies and Publishes 700+ Open Access Journals which contains over 50000 eminent personalities, reputed scientists as editorial board members.

Open Access Journals gaining more Readers and Citations

700 Journals and 15,000,000 Readers Each Journal is getting 25,000+ Readers

This Readership is 10 times more when compared to other Subscription Journals (Source: Google Analytics)

Original Articles Open Access


Parkinson’s disease (PD) is commonly characterized by motor movement deterioration and cognitive impairment. A dopamine-derived endogenous neurotoxin, namely salsolinol was found contributing to pathogenesis of the disease. However, the precise molecular mechanisms of the neurotoxin remain unexplored. Hence, this study aims to evaluate the effect of salsolinol on SH-SY5Y neuronal cells, focusing on oxidative stress-associated apoptotic cell death. Salsolinol was added to SH-SY5Y cells for determination of cell proliferation and viability using cell growth curve and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assays respectively. Cell cycle analysis was performed to measure cell cycle phase distribution while presence of apoptotic cell death was confirmed with Hoechst stain. Additionally, 2’,7’-dichlorofluorescein diacetate assay was carried out to investigate generation of reactive oxygen species (ROS) and enzyme-linked immunosorbent assay was performed to determine the expression of superoxide dismutase (SOD), NF-E2 related factor 2 (Nrf2) and kelch-like ECH-associated protein 1 (Keap1) proteins. Results reveal that SH-SY5Y cells, when treated with salsolinol (0-100 μM) for 24, 48 and 72 hours elicited neurotoxicity. The reduction and inhibition of cell growth and induction of apoptosis were coincided with enhanced ROS production and increased SOD, Nrf2 and Keap1 proteins expression. Thus, it is suggested that salsolinol can induce oxidative stress-associated apoptotic cell death via SOD, Nrf2 and Keap1 activation

To read the full article Peer-reviewed Article PDF image

Author(s): YiingJye Yap Raevathi Omasanggar Yuan Lin Koh Mei Yeng Yew Hien Tet LaiAnna Pick Kiong Ling Soi Moi Chye Khuen Yen Ng and Rhun Yian Koh


Parkinson’s disease, Salsolinol, Apoptosis, Oxidative stress, Nrf2-Keap1 pathway, signalling regulation

Peer Reviewed Journals
Make the best use of Scientific Research and information from our 700 + peer reviewed, Open Access Journals
International Conferences 2017-18
Meet Inspiring Speakers and Experts at our 3000+ Global Annual Meetings

Contact Us

Agri, Food, Aqua and Veterinary Science Journals

Dr. Krish

1-702-714-7001 Extn: 9040

Clinical and Biochemistry Journals

Datta A

1-702-714-7001Extn: 9037

Business & Management Journals


1-702-714-7001Extn: 9042

Chemical Engineering and Chemistry Journals

Gabriel Shaw

1-702-714-7001 Extn: 9040

Earth & Environmental Sciences

Katie Wilson

1-702-714-7001Extn: 9042

Engineering Journals

James Franklin

1-702-714-7001Extn: 9042

General Science and Health care Journals

Andrea Jason

1-702-714-7001Extn: 9043

Genetics and Molecular Biology Journals

Anna Melissa

1-702-714-7001 Extn: 9006

Immunology & Microbiology Journals

David Gorantl

1-702-714-7001Extn: 9014

Informatics Journals

Stephanie Skinner

1-702-714-7001Extn: 9039

Material Sciences Journals

Rachle Green

1-702-714-7001Extn: 9039

Mathematics and Physics Journals

Jim Willison

1-702-714-7001 Extn: 9042

Medical Journals

Nimmi Anna

1-702-714-7001 Extn: 9038

Neuroscience & Psychology Journals

Nathan T

1-702-714-7001Extn: 9041

Pharmaceutical Sciences Journals

John Behannon

1-702-714-7001Extn: 9007

Social & Political Science Journals

Steve Harry

1-702-714-7001 Extn: 9042

© 2008-2017 OMICS International - Open Access Publisher. Best viewed in Mozilla Firefox | Google Chrome | Above IE 7.0 version