fa 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 کارآزمایی بالینی Clinical Trials <strong><em>Background and Objective: </em></strong>Alzheimer&rsquo;s disease (<a name="OLE_LINK32"></a><a name="OLE_LINK31">AD</a>) 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 <a name="OLE_LINK110"></a><a name="OLE_LINK109"></a><a name="OLE_LINK108"></a><a name="OLE_LINK107">nicotinic acetylcholine receptors, protein kinase B (PKB) and protein kinase </a>M (PKM) were evaluated in order to examine the mechanism of the protective effects of rosmarinic acid in a rat model of Alzheimer&rsquo;s disease.<br> <strong><em>Materials and Methods:</em></strong> <a>Animals</a><a href="#_msocom_1" id="_anchor_1" name="_msoanchor_1">[vog1]</a>&nbsp; were divided into 6 groups consisting of 1) Sham, 2) Beta amyloid, <a name="OLE_LINK70"></a><a name="OLE_LINK69"></a><a name="OLE_LINK72"></a><a name="OLE_LINK71">3) Rosmarinic acid pretreated beta amyloid</a> (25 mg/kg), 4-6) <a name="OLE_LINK78"></a><a name="OLE_LINK77">Rosmarinic acid and </a>PKM inhibitor, PKB inhibitor and acetylcholine receptor inhibitor pretreated beta amyloid. <a name="OLE_LINK88"></a><a name="OLE_LINK87"></a><a name="OLE_LINK86"></a><a name="OLE_LINK85">Two weeks post-surgery, b</a><a name="OLE_LINK84"></a><a name="OLE_LINK83">ehavioral</a> (<a name="OLE_LINK226"></a><a name="OLE_LINK225">alternation percent in Y maze and step through latency in passive avoidance</a> task) and histochemical (hippocampal malondialdehyde and neuronal density measurement) studies were performed.<br> <strong><em>Results:</em></strong> <a name="OLE_LINK98"></a><a name="OLE_LINK97">Pretreatment of beta amyloid</a> 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).<br> <strong><em>Conclusion</em></strong>: Based on the findings of this study, it seems that in this experimental model of Alzheimer&rsquo;s <a name="OLE_LINK44"></a><a name="OLE_LINK43">disease</a> the protective effects of rosmarinic acid were derived from its antioxidant properties and partially via <a name="OLE_LINK128"></a><a name="OLE_LINK127">nicotinic acetylcholine receptors, PKB and </a>PKM. <div> <hr align="left" size="1" width="33%" > <div> <div id="_com_1"><a name="_msocom_1"></a><span dir="LTR">&nbsp;<a href="#_msoanchor_1">[vog1]</a></span><span dir="LTR">Which animals??</span><br> <span dir="LTR">How many???</span></div> </div> </div> Keywords: Rosmarinic acid, Oxidative stress, Nicotinic acetylcholine receptors, Protein kinase B, Protein kinase 43 57 http://journal.zums.ac.ir/browse.php?a_code=A-10-4-1046&slc_lang=fa&sid=1 Torandokht Baluchnejadmojarad تورانداخت بلوچ نژاد مجرد tmojarad@yahoo.com 5200319475328460052647 5200319475328460052647 Yes Dept. of Physiology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran دکترای تخصصی فیزیولوژی انسانی، استاد گروه فیزیولوژی، دانشکده‌ی پزشکی، دانشگاه علوم پزشکی ایران، تهران Mehrdad Roghani مهرداد روغنی 5200319475328460052648 5200319475328460052648 No Dept of Physiology, School of Medicine, Neurophysiology Research Center, Shahed University, Tehran, Iran دکترای تخصصی فیزیولوژی انسانی، استاد مرکز تحقیقات نوروفیزیولوژی، دانشگاه شاهد، تهران Parastoo Kazemloo پرستو کاظملو 5200319475328460052649 5200319475328460052649 No Dept of Physiology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran کارشناس ارشد فیزیولوژی، گروه فیزیولوژی، دانشکده‌ی پزشکی، دانشگاه علوم پزشکی ایران، تهران