CASPASE INHIBITION IN NEUROINFLAMMATION INDUCED BY SOLUBLE β AMYLOID MONOMER, PROTECTS CELLS FROM ABNORMAL SURVIVAL AND PROLIFERATION, VIA ATTENUATION OF NFKB ACTIVITY

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ABDI AZADEH; MOHAGHEGHI FATEMEH; SADRAIE SEYED HOMAYOON; DARGAHI LEILA; KHALAJ LEILA; AHMADIANI ABOLHASSAN

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Journal: Physiology and Pharmacology Year:2010 | Volume:14 | Issue:3 Page(s): 212-219

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Title

CASPASE INHIBITION IN NEUROINFLAMMATION INDUCED BY SOLUBLE β AMYLOID MONOMER, PROTECTS CELLS FROM ABNORMAL SURVIVAL AND PROLIFERATION, VIA ATTENUATION OF NFKB ACTIVITY

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Keywords

NEUROINFLAMMATIONQ2

APOPTOSISQ3

NF-KBQ3

CASPASE-3Q2

CELL PROLIFERATIONQ2

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-a 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 b–amyloid peptide (soluble Ab monomer) injection into the Wistar male rat prefrontal cortex for induction of NEUROINFLAMMATION in the hippocampus. Levels of TNF-a 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 b–amyloid peptide injection we observed an increase in TNF-a 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-kB was decreased and cytosolic NF-kB was increased and these changes were significant compared to Ab-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.

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APA: Copy

ABDI, AZADEH, MOHAGHEGHI, FATEMEH, SADRAIE, SEYED HOMAYOON, DARGAHI, LEILA, KHALAJ, LEILA, & AHMADIANI, ABOLHASSAN. (2010). CASPASE INHIBITION IN NEUROINFLAMMATION INDUCED BY SOLUBLE β AMYLOID MONOMER, PROTECTS CELLS FROM ABNORMAL SURVIVAL AND PROLIFERATION, VIA ATTENUATION OF NFKB ACTIVITY. PHYSIOLOGY AND PHARMACOLOGY, 14(3), 212-219. SID. https://sid.ir/paper/75188/en

Vancouver: Copy

ABDI AZADEH, MOHAGHEGHI FATEMEH, SADRAIE SEYED 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 NFKB ACTIVITY. PHYSIOLOGY AND PHARMACOLOGY[Internet]. 2010;14(3):212-219. Available from: https://sid.ir/paper/75188/en

IEEE: Copy

AZADEH ABDI, FATEMEH MOHAGHEGHI, SEYED HOMAYOON SADRAIE, LEILA DARGAHI, LEILA KHALAJ, and ABOLHASSAN AHMADIANI, “CASPASE INHIBITION IN NEUROINFLAMMATION INDUCED BY SOLUBLE β AMYLOID MONOMER, PROTECTS CELLS FROM ABNORMAL SURVIVAL AND PROLIFERATION, VIA ATTENUATION OF NFKB ACTIVITY,” PHYSIOLOGY AND PHARMACOLOGY, vol. 14, no. 3, pp. 212–219, 2010, [Online]. Available: https://sid.ir/paper/75188/en

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