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 | Volume 14, Number 3 (Fall 2010 2010) |  | |
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 | Caspase inhibition in neuroinflammation induced by soluble β amyloid monomer, protects cells from abnormal survival and proliferation, via attenuation of NFқB activity |  |
| | Author(s): Azadeh Abdi, Fatemeh Mohagheghi, Homayoon Sadraei, Leila Dargahi, Leila Khalaj and Abolhassan Ahmadiani | | | Study Type: Original Research | Subject: Pharmacology | | | Article abstract: | | Introduction: Evidence suggests that 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. Since TNF-α is able to induce apoptosis as
well as increased viability of the cells by activation of caspases or NF-kB, respectively, the question is what will happen
if the balance between the two pathways is disturbed by inhibition of apoptosis.
Methods: In this study, we used β–amyloid peptide (soluble Aβ monomer) injection into the Wistar male rat
prefrontal cortex for induction of neuroinflammation in the hippocampus. Levels of TNF-α and caspase-3 were
determined via western blot analysis. 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 was
evaluated via western blotting.
Results: After β–amyloid peptide injection we observed an increase in TNF-α and caspase3 as an inflammatory
cytokine and apoptotic marker, respectively (P<0.001 and P<0.0001, respectively). As a consequences of apoptosis
inhibition, nuclear NF-κB was decreased and cytosolic NF-κB was increased and these changes were significant
compared to Aβ-injected group (P<0.001 and P<0.05, respectively).
Conclusion: Caspase inhibition as an initiator of apoptosis, probably by attenuation of NF-kB activity, protect cells
from abnormal survival and proliferation. | | | Keywords: neuroinflammation, apoptosis, NF-κB, caspase-3, cell proliferation, | |
| Full text [PDF 663 kb] | | | |
| | How to cite this article | Download citation data for: BibTeX | EndNote | Medlars | ProCite | Reference Manager | RefWorks |
Send citation data to: CiteULike | RefWorks | | Abdi Azadeh, Mohagheghi Fatemeh, Sadraei Homayoon, Dargahi Leila, Khalaj Leila, Ahmadiani Abolhassan, Caspase inhibition in neuroinflammation induced by soluble β amyloid monomer, protects cells from abnormal survival and proliferation, via attenuation of NFқB activity Physiology and Pharmacology, 2010; 14 (3) :211-219 URL http://www.phypha.ir/ppj/browse.php?a_code=A-10-335-2&slc_lang=en&sid=1 | | |
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| Address: Neuroscience Research Center, P.O.Box: 19615-1178, I.R.Iran, Fax:+98-21-22431624, Tel:+98-21-22429765-7. | |
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