Paper Information

Title: 

APOPTOSIS INHIBITION CAN BE THREATENING IN Aβ-INDUCED NEUROINFLAMMATION, THROUGH PROMOTING CELL PROLIFERATION

Type: POSTER
Author(s): ABDI AZADEH*,SADRAEI H.,DARGAHI L.,KHALAJ L.,AHMADIAN ABOU ALHASAN
 
 *NEUROSCIENCE RESEARCH CENTER AND DEPARTMENT OF PHARMACOLOGY, SCHOOL OF MEDICINE, SHAHID BEHESHTI UNIVERSITY OF MEDICAL SCIENCES, TEHRAN, IRAN
 
Name of Seminar: IRANIAN CONGRESS OF PHYSIOLOGY AND PHARMACOLOGY
Type of Seminar:  CONGRESS
Sponsor:  PHYSIOLOGY AND PHARMACOLOGY SOCIETY, MASHHAD UNIVERSITY OF MEDICAL SCIENCE
Date:  2009Volume 19
 
 
Abstract: 

Evidence suggests neuronal apoptosis in neurodegenerative diseases is correlated with inflammatory reactions. The beneficial or detrimental role of apoptosis in neuroinflammation is unclear. Elucidating this question may be helpful in management of neurodegenerative diseases. In this study, we used b–amyloid peptide (Ab) injection into the rat prefrontal cortex for induction of neuroinflammation in hippocampus. We observed an increase in TNF-α and aspase3 as an inflammatory cytokine and apoptotic marker, respectively. Apoptosis was confirmed by TUNEL assay. As far as ability of TNF-a to induce apoptosis or activate NF-kb, the question is what will happen if the balance between two pathways be disturbed by inhibition of apoptosis. Using chronic intracerebroventricular administration of caspase inhibitors, z-VAD –fmk and z DEVD-fmk, we inhibited apoptosis. Exploring consequences of apoptosis inhibition, activity of NF-kb and expression of Hsp 70 as a hallmark of cancer that is upregulated by stress and toxicants, cmyc as a proto-oncogene and p53 as a tumor suppressor protein were evaluated. There was an unexpected decrease in NF-kb activity while Hsp 70 and cmyc upregulated and p53 decreased. These results imply that inhibition of apoptosis due to increased susceptibility to abnormal mitosis may not provide a reliable strategy for treatment of neuroinflammatory diseases.

 
Keyword(s): NEUROINFLAMMATION, APOPTOSIS, NF-Κβ, CASPASE-3, CELL PROLIFERATION
 
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