alexa The Ginkgo biloba extract (EGb 761) protects hippocampal neurons against cell death induced by beta-amyloid.
Pharmaceutical Sciences

Pharmaceutical Sciences

Clinical Pharmacology & Biopharmaceutics

Author(s): Bastianetto S, Ramassamy C, Dor S, Christen Y, Poirier J,

Abstract Share this page

Abstract Substantial evidence suggests that the accumulation of beta-amyloid (Abeta)-derived peptides, and to a lesser extent free radicals, may contribute to the aetiology and/or progression of Alzheimer's disease (AD). Ginkgo biloba extract (EGb 761) is a well-defined plant extract containing two major groups of constituents, i.e. flavonoids and terpenoids. It is viewed as a polyvalent agent with a possible therapeutic use in the treatment of neurodegenerative diseases of multifactorial origin, e.g. AD. We have investigated here the potential effectiveness of EGb 761 against toxicity induced by (Abeta)-derived peptides (Abeta25-35, Abeta1-40 and Abeta1-42) on hippocampal primary cultured cells, this area being severely affected in AD. A co-treatment with EGb 761 concentration-dependently (10-100 microg/mL) protected hippocampal neurons against toxicity induced by Abeta fragments, with a maximal and complete protection at the highest concentration tested. Similar, albeit less potent protective effects were seen with the flavonoid fraction of the extract (CP 205), while the terpenes were ineffective. Most interestingly, EGb 761 (100 microg/mL) was even able to protect (up to 8 h) hippocampal cells from a pre-exposure to Abeta25-35 and Abeta1-40. EGb 761 was also able to both protect and rescue hippocampal cells from toxicity induced by H2O2 (50-150 microM), a major peroxide possibly involved in mediating Abeta toxicity. Moreover, EGb 761 (10-100 microg/mL), and to a lesser extent CP 205 (10-50 microg/mL), completely blocked Abeta-induced events, e.g. reactive oxygen species accumulation and apoptosis. These results suggest that the neuroprotective effects of EGb 761 are partly associated with its antioxidant properties and highlight its possible effectiveness in neurodegenerative diseases, e.g. AD via the inhibition of Abeta-induced toxicity and cell death.
This article was published in Eur J Neurosci and referenced in Clinical Pharmacology & Biopharmaceutics

Relevant Expert PPTs

Relevant Speaker PPTs

Relevant Topics

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 & Aquaculture Journals

Dr. Krish

1-702-714-7001Extn: 9040

Biochemistry Journals

Datta A

1-702-714-7001Extn: 9037

Business & Management Journals


1-702-714-7001Extn: 9042

Chemistry Journals

Gabriel Shaw

1-702-714-7001Extn: 9040

Clinical Journals

Datta A

1-702-714-7001Extn: 9037

Engineering Journals

James Franklin

1-702-714-7001Extn: 9042

Food & Nutrition Journals

Katie Wilson

1-702-714-7001Extn: 9042

General Science

Andrea Jason

1-702-714-7001Extn: 9043

Genetics & Molecular Biology Journals

Anna Melissa

1-702-714-7001Extn: 9006

Immunology & Microbiology Journals

David Gorantl

1-702-714-7001Extn: 9014

Materials Science Journals

Rachle Green

1-702-714-7001Extn: 9039

Nursing & Health Care Journals

Stephanie Skinner

1-702-714-7001Extn: 9039

Medical Journals

Nimmi Anna

1-702-714-7001Extn: 9038

Neuroscience & Psychology Journals

Nathan T

1-702-714-7001Extn: 9041

Pharmaceutical Sciences Journals

Ann Jose

1-702-714-7001Extn: 9007

Social & Political Science Journals

Steve Harry

1-702-714-7001Extn: 9042

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