Document Detail

Attenuation of Aβ-induced neurotoxicity by thymoquinone via inhibition of mitochondrial dysfunction and oxidative stress.
MedLine Citation:
PMID:  22752387     Owner:  NLM     Status:  MEDLINE    
Beta-amyloid (Aβ) peptides are considered to play a major role in the pathogenesis of Alzheimer's disease (AD) and compounds that can prevent pathways of Aβ-induced neurotoxicity may be potential therapeutic agents for treatment of AD. This study examined the hypothesis that thymoquinone (TQ) would reduce oxidative stress and mitochondrial dysfunction in differentiated pheochromocytoma (PC 12) cells exposed to Aβ fragment 25-35 (Aβ(25-35)). To test this hypothesis, Aβ was used to induce an in vitro model of AD in differentiated PC 12 cell line of rat. After 24 h of exposure with Aβ(25-35), a significant reduction in cell viability and mitochondrial membrane potential (MMP) was observed. In addition, a significant elevation in the TBARS content and nitric oxide (NO) and activity of acetylcholine esterase (AChE) was observed which was restored significantly by TQ pretreatment. Furthermore, TQ also ameliorated glutathione and its dependent enzymes (glutathione peroxidase, glutathione reductase) which were depleted by Aβ(25-35) in PC 12 cells. These results were supported by the immunocytochemical finding that has shown protection of cells by TQ from noxious effects of Aβ(25-35). These results indicate that TQ holds potential for neuroprotection and may be a promising approach for the treatment of neurodegenerative disorders including AD.
Andleeb Khan; Kumar Vaibhav; Hayate Javed; Mohd Moshahid Khan; Rizwana Tabassum; Md Ejaz Ahmed; Pallavi Srivastava; Gulrana Khuwaja; Farah Islam; Mohd Saeed Siddiqui; Mohammed M Safhi; Mohammed M Shafi; Fakhrul Islam
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2012-07-01
Journal Detail:
Title:  Molecular and cellular biochemistry     Volume:  369     ISSN:  1573-4919     ISO Abbreviation:  Mol. Cell. Biochem.     Publication Date:  2012 Oct 
Date Detail:
Created Date:  2012-08-28     Completed Date:  2013-04-10     Revised Date:  2013-10-17    
Medline Journal Info:
Nlm Unique ID:  0364456     Medline TA:  Mol Cell Biochem     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  55-65     Citation Subset:  IM    
Department of Medical Elementology and Toxicology (Fund for the Improvement of Science and Technology Sponsored by DST and Special Assistance Programme Sponsored by UGC), Jamia Hamdard (Hamdard University), Hamdard Nagar, New Delhi, India.
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MeSH Terms
Acetylcholinesterase / metabolism
Alzheimer Disease / drug therapy
Amyloid beta-Peptides* / antagonists & inhibitors,  toxicity
Apoptosis / drug effects
Benzoquinones / administration & dosage*
Cell Survival / drug effects*
Glutathione Peroxidase / metabolism
Membrane Potential, Mitochondrial / drug effects
Mitochondria* / drug effects,  pathology
Neuroprotective Agents / administration & dosage*
Nitric Oxide / metabolism
Oxidative Stress / drug effects
PC12 Cells
Peptide Fragments* / antagonists & inhibitors,  toxicity
Thiobarbituric Acid Reactive Substances / metabolism
Reg. No./Substance:
0/Amyloid beta-Peptides; 0/Benzoquinones; 0/Neuroprotective Agents; 0/Peptide Fragments; 0/Thiobarbituric Acid Reactive Substances; 0/amyloid beta-protein (25-35); 10102-43-9/Nitric Oxide; 490-91-5/thymoquinone; EC Peroxidase; EC
Erratum In:
Mol Cell Biochem. 2013 Apr;376(1-2):197
Note: Shafi, Mohammed M [corrected to Safhi, Mohammed M]

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