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Paper Information

Title: 

CANNABINOIDS PREVENT THE INDUCTION OF APOPTOSIS IN A RAT MODEL OF ALZHEIMER’S DISEASE

Type: SPEECH
Author(s): HAGHANI MASOUD,JAVAN M.,SHAABANI MOHAMMAD,JANAHMADI M.2
 
 
 
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: 

b-amyloid (Ab) peptide aggregation represents a pivotal event in the neuronal apoptosis occurring in Alzheimer’s disease (AD). Here, the possible neuroprotective effect of cannabinoids receptors against Ab -induced apoptosis was investigated. To induce an AD model, Ab 1-42 was injected bilaterally into the prefrontal cortex (30ng /side). WIN 55, 212-2, a non-selective cannabinoid receptor agonist, ACEA and AM251 (CB1 receptor agonist and antagonist, respectively) and AM630 (a CB2 receptor antagonist) were injected 6 h after the local injection of Ab in different groups. The treatment was repeated daily for a period of 12 days, when rats were sacrificed. Western blotting was used to evaluate the expression of two proteins involved in the activation of apoptotic pathways and neuroprotection after Aβ- induced neurotoxicity: caspase 3 and calbindin, respectively. Neuronal apoptosis was detected in hippocampal regions of rats inoculated with Ab alone. Findings showed a significant increase in capsase-3, and a small but not statistically significant decrease in calbindin and pro-caspase in Ab -treated rats. Following WIN+Ab administration, the induction of apopotosis by Aβ was reduced by 47% compared to Ab -treated rats. The protective effect of cannabinoids was also confirmed by ACEA treatment, which reduced the caspase-3 level by 27.5%. Both the protective effects of WIN55, 212-2 and ACEA were abolished by AM251, suggesting that the neuroprotection is mediated by CB1 cannabinoid receptors. On the other hand, although treatments did not cause a significant change in calbindin level, but there was a significant negative correlation between calbindin and capsae-3 in all experimental groups.

 
Keyword(s): ALZHEIMER, Β-AMYLOID ,CANNABINOIDS,NEUROPROTECTIVE,CASPASE 3
 
 
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