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Reduction of Autophagy Markers Mediated Protective Effects of Jnk Inhibitor and Bucladesine on Memory Deficit Induced by Aβ in Rats Publisher Pubmed



Mohammadi M1 ; Guan J2, 3, 4 ; Khodagholi F5, 6 ; Yans A5, 6 ; Khalaj S1 ; Gholami M1 ; Taghizadeh GH1, 7 ; Aliaghaei A8 ; Abdollahi M1 ; Ghahremani MH1 ; Sharifzadeh M1, 7
Authors
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Authors Affiliations
  1. 1. Department of Pharmacology and Toxicology, Pharmaceutical Sciences Research Centre, Faculty of Pharmacy, Tehran University of Medical Sciences, P.O. Box 14155-6451, Tehran, Iran
  2. 2. Liggins Institute, University of Auckland, 85 Park Road, Grafton, Auckland, New Zealand
  3. 3. Centre for Brain Research, Faculty of Medicine and Health Sciences, University of Auckland, 85 Park Road, Grafton, Auckland, New Zealand
  4. 4. Gravida National Centre for Growth and Development, University of Auckland, Auckland, New Zealand
  5. 5. Neuroscience Research Centre, ShahidBeheshti University of Medical Sciences, Tehran, Iran
  6. 6. Neurobiology Research Centre, ShahidBeheshti University of Medical Sciences, Tehran, Iran
  7. 7. Department of Neuroscience, Faculty of Advanced Science and Technology in Medicine, Tehran University of Medical Sciences, Tehran, Iran
  8. 8. Department of Anatomy and Cell Biology, School of Medicine, ShahidBeheshti University of Medical Sciences, Tehran, Iran

Source: Naunyn-Schmiedeberg's Archives of Pharmacology Published:2016


Abstract

Autophagy, the process of self-degradation of cellular components, has an important role in neurodegenerative diseases, such as Alzheimer's disease. In this study, we investigated the effects of SP600125 as c-Jun N-terminal kinase (JNK) inhibitor and bucladesine as a cyclic adenosine 3′,5′-monophosphate (cAMP) analog on spatial memory and expression of autophagic factors in Aβ-injected rats. Male Wistar rats were used. Rats were randomly allocated into five groups as following: amyloid beta (Aβ)-only group, Aβ + SP600125 (30 μg/1 μ/side, n = 7) and/or bucladesine (100 μM/1 μl/side, n = 7), and the normal control (vehicle only) group. The treatments were administered bilaterally to the CA1 sub-region of the hippocampus stereotaxically. Spatial reference memory was performed using Morris Water Maze 21 days later. The expression of authophagy markers (beclin1, Atg7, Atg12, and LC3 II/LC3 I) in the hippocampus was evaluated using western blotting. Compared to the vehicle group, Aβ administration reduced spatial reference learning (P < 0.001) and memory (P < 0.01) and upregulated the expression of beclin1, Atg7, Atg12, and LC3 II/I (P < 0.0001). Compare to Aβ-only group, the administration of SP600125 and/or bucladesine improved spatial reference learning (P < 0.001) and memory (P < 0.01). Compared to the Aβ-only group, the treatment with SP600125 and/or bucladesine also reduced beclin1, Atg7, Atg12, and LC3 II/I (P < 0.0001) which was similar to amount of normal rats. In summary, it seems that the improvement of spatial memory by SP600125 and/or bucladesine in Aβ-injected rats is in relation with normalizing of autophagy to the physiologic level, possibly through neuroprotection and/or neuroplasticity. © 2016 Springer-Verlag Berlin Heidelberg.
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