<?xml version="1.0" encoding="utf-8"?>
<journal>
<title>Journal of Advances in Medical and Biomedical Research</title>
<title_fa>Journal of Advances in Medical and Biomedical Research</title_fa>
<short_title>J Adv Med Biomed Res</short_title>
<subject>Medical Sciences</subject>
<web_url>http://journal.zums.ac.ir</web_url>
<journal_hbi_system_id>52</journal_hbi_system_id>
<journal_hbi_system_user>journal52</journal_hbi_system_user>
<journal_id_issn>1606-9366</journal_id_issn>
<journal_id_issn_online>2676-6264</journal_id_issn_online>
<journal_id_pii></journal_id_pii>
<journal_id_doi>10.30699/jambr</journal_id_doi>
<journal_id_iranmedex></journal_id_iranmedex>
<journal_id_magiran></journal_id_magiran>
<journal_id_sid></journal_id_sid>
<journal_id_nlai></journal_id_nlai>
<journal_id_science></journal_id_science>
<language>en</language>
<pubdate>
	<type>jalali</type>
	<year>1396</year>
	<month>3</month>
	<day>1</day>
</pubdate>
<pubdate>
	<type>gregorian</type>
	<year>2017</year>
	<month>6</month>
	<day>1</day>
</pubdate>
<volume>25</volume>
<number>111</number>
<publish_type>online</publish_type>
<publish_edition>1</publish_edition>
<article_type>fulltext</article_type>
<articleset>
	<article>


	<language>fa</language>
	<article_id_doi></article_id_doi>
	<title_fa>تأثیر آنتی-آپوپتوتیک سلژلین به‌عنوان بازدارنده‌ی مونو آمین اکسیداز بر سلول‌های بنیادی عصبی مشتق شده از هیپوکمپ موش صحرایی در شرایط آسیب اکسیداتیو</title_fa>
	<title>Anti-Apoptotic Effect of Selegiline as Monoamine Oxidase Inhibitor on Rat Hippocampus Derived Neural Stem Cells in Oxidative Stress Condition</title>
	<subject_fa></subject_fa>
	<subject></subject>
	<content_type_fa>کارآزمایی بالینی</content_type_fa>
	<content_type>Clinical Trials</content_type>
	<abstract_fa></abstract_fa>
	<abstract>&lt;p style=&quot;text-align: justify;&quot;&gt;&lt;strong&gt;&lt;em&gt;Background and Objective:&lt;/em&gt;&lt;/strong&gt; Damaged and inflammatory cells in the nervous system produce reactive oxygen species (ROS). The overproduction of ROS can cause serious damage to important biomolecules and over activation of programmed cell death leads to many progressive neurodegenerative disorders. The aim of this study was to evaluate the effects of selegiline on inhibition of apoptosis in oxidative damage induced by hydrogen peroxide in rat hippocampus derived neural stem cells.&lt;/p&gt;

&lt;p style=&quot;text-align: justify;&quot;&gt;&lt;strong&gt;&lt;em&gt;Materials and Methods:&lt;/em&gt;&lt;/strong&gt; The neural stem cells were isolated from the hippocampi of neonatal rats then pretreated with different doses of selegiline for 48 hours while later being exposed to 125&amp;mu;M H2O2 for 30 min. Using MTT assay and TUNEL staining, we evaluated the effects of selegiline on cell survival and apoptosis in pretreated NSCs compared to control groups. Also, the induction of NSCs to neuron-like cells was evaluated using Nissl staining.&lt;/p&gt;

&lt;p style=&quot;text-align: justify;&quot;&gt;&lt;strong&gt;&lt;em&gt;Results: &lt;/em&gt;&lt;/strong&gt;The results showed that apoptosis rate was significantly decreased in 10&lt;sup&gt;-7&lt;/sup&gt; M of selegiline pretreated NSCs compared to the control group. Also, the mean percentage of Nissl positive cells significantly increased in selegiline pretreated neural stem cells compared to the control group.&lt;/p&gt;

&lt;p style=&quot;text-align: justify;&quot;&gt;&lt;strong&gt;&lt;em&gt;Conclusion:&lt;/em&gt;&lt;/strong&gt; Our findings suggest that selegiline protects NSCs against oxidative stress induced cell death, and therefore, it may be used to promote the survival rate of NSCs and can be a candidate for treatment of oxidative stress-mediated neurological diseases.&lt;/p&gt;
&lt;p&gt;&lt;/p&gt;&lt;p&gt;&lt;/p&gt;</abstract>
	<keyword_fa></keyword_fa>
	<keyword>Neural stem cells, Selegiline, Oxidative stress, Apoptosis</keyword>
	<start_page>41</start_page>
	<end_page>56</end_page>
	<web_url>http://journal.zums.ac.ir/browse.php?a_code=A-10-4-1022&amp;slc_lang=fa&amp;sid=1</web_url>


<author_list>
	<author>
	<first_name>Ali</first_name>
	<middle_name></middle_name>
	<last_name>Nikfar </last_name>
	<suffix></suffix>
	<first_name_fa>علی</first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa>نیک فر</last_name_fa>
	<suffix_fa></suffix_fa>
	<email></email>
	<code>5200319475328460053259</code>
	<orcid>5200319475328460053259</orcid>
	<coreauthor>No</coreauthor>
	<affiliation>Dept. of Genetics and Molecular Medicine, Faculty of Medicine, Zanjan University of Medical Sciences, Zanjan, Iran.</affiliation>
	<affiliation_fa>دانشکده پزشکی، دانشگاه علوم پزشکی زنجان، زنجان</affiliation_fa>
	 </author>


	<author>
	<first_name>Alireza</first_name>
	<middle_name></middle_name>
	<last_name>Abdanipour </last_name>
	<suffix></suffix>
	<first_name_fa>علیرضا</first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa>عبدانی پور</last_name_fa>
	<suffix_fa></suffix_fa>
	<email></email>
	<code>5200319475328460053260</code>
	<orcid>5200319475328460053260</orcid>
	<coreauthor>Yes
</coreauthor>
	<affiliation></affiliation>
	<affiliation_fa>دانشکده پزشکی، دانشگاه علوم پزشکی زنجان، زنجان</affiliation_fa>
	 </author>


	<author>
	<first_name>Masoumeh</first_name>
	<middle_name></middle_name>
	<last_name>Gholinejad </last_name>
	<suffix></suffix>
	<first_name_fa>معصومه</first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa>قلی نژاد</last_name_fa>
	<suffix_fa></suffix_fa>
	<email></email>
	<code>5200319475328460053261</code>
	<orcid>5200319475328460053261</orcid>
	<coreauthor>No</coreauthor>
	<affiliation>Dept. of Medical Biotechnology and Nanotechnology, Faculty of Medicine, Zanjan University of Medical Sciences, Zanjan, Iran.</affiliation>
	<affiliation_fa>دانشکده پزشکی، دانشگاه علوم پزشکی زنجان، زنجان</affiliation_fa>
	 </author>


</author_list>


	</article>
</articleset>
</journal>
