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Reduction of autophagy markers mediated protective effects of JNK inhibitor and bucladesine on memory deficit induced by Aβ in rats.

Naunyn Schmiedebergs Arch Pharmacol.. 2016-05; 
Mohammadi M, Guan J,Khodagholi F,Yans A,Khalaj S, Gholami M, Taghizadeh GH,Aliaghaei A, Abdollahi M, Ghahremani MH, Sharifzadeh M.
Products/Services Used Details Operation
Catalog Products ... SP600125 and bucladesine were purchased from Sigma-Aldrich (St. Louis, MO, USA). Aβ 1–42 was purchased from Genscript (NJ, USA). Aliquots of Aβ 1–42 at a concentration of 1000 ng/μl were prepared and were stored at −20 °C until use. ... Get A Quote

摘要

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 t... More

关键词

Alzheimer disease; Amyloid beta (Aβ); Autophagy; Bucladesine; SP600125