چهارشنبه 15 اسفند 1403
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دوره 25، شماره 113 - ( 6-1396 )
جلد 25 شماره 113 صفحات 57-43 |
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Baluchnejadmojarad T, Roghani M, Kazemloo P. The Role of Acetylcholine Nicotinic Receptors, Protein Kinase B and Protein Kinase M on the Protective Effect of Rosmarinic Acid in Beta Amyloid (25-35) Induced Rat Model of Alzheimer’s Disease. J Adv Med Biomed Res 2017; 25 (113) :43-57
URL: http://journal.zums.ac.ir/article-1-4792-fa.html
URL: http://journal.zums.ac.ir/article-1-4792-fa.html
بلوچ نژاد مجرد تورانداخت، روغنی مهرداد، کاظملو پرستو. نقش گیرنده‌های نیکوتینی استیل کولین، پروتئین کیناز B و پروتئین کیناز Mζ بر اثر حفاظتی اسید رزمارینیک در مدل بیماری آلزایمر القا شده به وسیله‌ی بتا آمیلوئید (35-25) در موش صحرایی. Journal of Advances in Medical and Biomedical Research. 1396; 25 (113) :43-57
1- دکترای تخصصی فیزیولوژی انسانی، استاد گروه فیزیولوژی، دانشکده‌ی پزشکی، دانشگاه علوم پزشکی ایران، تهران ، tmojarad@yahoo.com
2- دکترای تخصصی فیزیولوژی انسانی، استاد مرکز تحقیقات نوروفیزیولوژی، دانشگاه شاهد، تهران
3- کارشناس ارشد فیزیولوژی، گروه فیزیولوژی، دانشکده‌ی پزشکی، دانشگاه علوم پزشکی ایران، تهران
2- دکترای تخصصی فیزیولوژی انسانی، استاد مرکز تحقیقات نوروفیزیولوژی، دانشگاه شاهد، تهران
3- کارشناس ارشد فیزیولوژی، گروه فیزیولوژی، دانشکده‌ی پزشکی، دانشگاه علوم پزشکی ایران، تهران
چکیده: (155665 مشاهده)
Background and Objective: Alzheimer’s disease (AD) is one of the most common neurodegenerative diseases and results from the extracellular accumulation of b-amyloid peptides and the resulting neuronal dysfunction. In this study, the role of nicotinic acetylcholine receptors, protein kinase B (PKB) and protein kinase M (PKM) were evaluated in order to examine the mechanism of the protective effects of rosmarinic acid in a rat model of Alzheimer’s disease.
Materials and Methods: Animals[vog1] were divided into 6 groups consisting of 1) Sham, 2) Beta amyloid, 3) Rosmarinic acid pretreated beta amyloid (25 mg/kg), 4-6) Rosmarinic acid and PKM inhibitor, PKB inhibitor and acetylcholine receptor inhibitor pretreated beta amyloid. Two weeks post-surgery, behavioral (alternation percent in Y maze and step through latency in passive avoidance task) and histochemical (hippocampal malondialdehyde and neuronal density measurement) studies were performed.
Results: Pretreatment of beta amyloid animals with rosmarinic acid considerably alleviated the behavioral and histochemical disturbances related to the hippocampus. In this group, nicotinic acetylcholine receptors and PKB inhibitors decreased step through latency (p<0.001) and increased hippocampal malondialdehyde levels (p<0.001). In addition, PKB inhibitors decreased hippocampal neuronal density in rosmarinic acid pretreated beta amyloid rats (p<0.05).
Conclusion: Based on the findings of this study, it seems that in this experimental model of Alzheimer’s disease the protective effects of rosmarinic acid were derived from its antioxidant properties and partially via nicotinic acetylcholine receptors, PKB and PKM.
Materials and Methods: Animals[vog1] were divided into 6 groups consisting of 1) Sham, 2) Beta amyloid, 3) Rosmarinic acid pretreated beta amyloid (25 mg/kg), 4-6) Rosmarinic acid and PKM inhibitor, PKB inhibitor and acetylcholine receptor inhibitor pretreated beta amyloid. Two weeks post-surgery, behavioral (alternation percent in Y maze and step through latency in passive avoidance task) and histochemical (hippocampal malondialdehyde and neuronal density measurement) studies were performed.
Results: Pretreatment of beta amyloid animals with rosmarinic acid considerably alleviated the behavioral and histochemical disturbances related to the hippocampus. In this group, nicotinic acetylcholine receptors and PKB inhibitors decreased step through latency (p<0.001) and increased hippocampal malondialdehyde levels (p<0.001). In addition, PKB inhibitors decreased hippocampal neuronal density in rosmarinic acid pretreated beta amyloid rats (p<0.05).
Conclusion: Based on the findings of this study, it seems that in this experimental model of Alzheimer’s disease the protective effects of rosmarinic acid were derived from its antioxidant properties and partially via nicotinic acetylcholine receptors, PKB and PKM.
نوع مطالعه: کارآزمایی بالینی |
دریافت: 1396/6/4 | پذیرش: 1396/6/4 | انتشار: 1396/6/4
دریافت: 1396/6/4 | پذیرش: 1396/6/4 | انتشار: 1396/6/4
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