Title of article :
Ellagic acid attenuates enhanced acetylcholinesterase reactivity in an experimental model of Alzheimer′s disease induced by beta amyloid25-35 in the rat
Author/Authors :
Kiasalari، Zahra نويسنده هييت علمي Kiasalari, Zahra , Khalili، Mohsen نويسنده , , Heydarifard، Rana نويسنده School of Medicine, Shahed University, Tehran, Iran , , Roghani، Mehrdad نويسنده Neurophysiology Research Center, Shahed University, Tehran, Iran ,
Issue Information :
دوفصلنامه با شماره پیاپی سال 2016
Pages :
4
From page :
23
To page :
26
Abstract :
Background and Objective: Alzheimer’s disease (AD) is a multifactorial disease with debilitating consequences and few therapeutic strategies exist for it. With regard to antioxidant capacity and anti-B-amyloid polymerization potential of ellagic acid, this study was conducted to evaluate the effect of this substance on enhanced acetylcholinesterase reactivity in an experimental model of Alzheimer?s disease induced by beta amyloid25-35 in the rat. Materials and Methods: In this experimental study, 32 male Wistar rats were divided into 4 equal groups, i.e. sham, treated-sham, Alzheimeric, and treated-Alzheimeric. For induction of AD, 2 µl of B-amyloid 25-35 (10 µg/2 µl) was microinjected bilaterally into CA1 of the dorsal hippocampus. The daily treatment with ellagic acid was done for one week at a dose of 100 mg/kg (i.p.) till 1 h pre-surgery. At third week after surgery, histochemistry for acetylcholinesterase reactivity was performed. Results: Alzheimeric group showed enhanced reactivity for acetylcholinesterase in dorsal hippocampus that was significant as compared to sham group (p < 0.005) and treatment of Alzheimeric rats with ellagic acid significantly prevented this abnormal change versus Alzheimeric group (p < 0.05). There was also no significant change in ellagic acid-treated sham group versus sham regarding acetylcholinesterase reactivity. Conclusion: Pretreatment of beta amyloid-induced-Alzheimeric rats by ellagic acid could ameliorate acetylcholinesterase reactivity in the dorsal hippocampus and this could possibly improve memory deterioration in AD.
Journal title :
Journal of Basic and Clinical Pathophysiology
Serial Year :
2016
Journal title :
Journal of Basic and Clinical Pathophysiology
Record number :
2404536
Link To Document :
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