<?xml version="1.0" encoding="utf-8"?>
<journal>
<title>Medical Journal of the Islamic Republic Of Iran</title>
<title_fa>مجله پزشکی جمهوری اسلامی ایران</title_fa>
<short_title>Med J Islam Repub Iran</short_title>
<subject>Medical Sciences</subject>
<web_url>http://mjiri.iums.ac.ir</web_url>
<journal_hbi_system_id>2</journal_hbi_system_id>
<journal_hbi_system_user>journal2</journal_hbi_system_user>
<journal_id_issn>1016-1430</journal_id_issn>
<journal_id_issn_online>2251-6840</journal_id_issn_online>
<journal_id_pii>8</journal_id_pii>
<journal_id_doi>10.18869/mjiri</journal_id_doi>
<journal_id_iranmedex></journal_id_iranmedex>
<journal_id_magiran></journal_id_magiran>
<journal_id_sid>14</journal_id_sid>
<journal_id_nlai>8888</journal_id_nlai>
<journal_id_science>13</journal_id_science>
<language>en</language>
<pubdate>
	<type>jalali</type>
	<year>1398</year>
	<month>11</month>
	<day>1</day>
</pubdate>
<pubdate>
	<type>gregorian</type>
	<year>2020</year>
	<month>2</month>
	<day>1</day>
</pubdate>
<volume>34</volume>
<number>1</number>
<publish_type>online</publish_type>
<publish_edition>1</publish_edition>
<article_type>fulltext</article_type>
<articleset>
	<article>


	<language>en</language>
	<article_id_doi></article_id_doi>
	<title_fa></title_fa>
	<title>Synovial interlukin-6 affects apoptosis induction via nuclear factor kappa-B and fractalkine pathway during adjuvant arthritis</title>
	<subject_fa>Physiology</subject_fa>
	<subject>Physiology</subject>
	<content_type_fa>Original Research</content_type_fa>
	<content_type>Original Research</content_type>
	<abstract_fa></abstract_fa>
	<abstract>&lt;strong&gt;Abstract&lt;/strong&gt;&lt;br&gt;
&lt;strong&gt;Background and objectives:&lt;/strong&gt; Apoptosis disruptions play substantial roles in pathogenesis of arthritis and its symptoms. Cytokines and their intra-cellular signaling have pivotal roles in arthritis pathophysiology. The present study aimed to investigate the relation between synovial Interleukin- 6 (IL-6), Nuclear Factor Kappa- B (NF-ĸB) and Fractalkine (Fkn) in the changes of edema and apoptosis during Adjuvant-induced knee arthritis.&lt;br&gt;
&lt;strong&gt;Methods:&lt;/strong&gt; 240 male Wistar rats were divided into different groups. Arthritis was evoked and the knee edema changes were evaluated by Vernier caliper. Synovial IL-6 was assayed by rat standard ELISA kit. Synovial NF-ĸB, Fkn, and markers of apoptosis were measured by western blot experiment.&lt;br&gt;
&lt;strong&gt;Results:&lt;/strong&gt; The injection of Complete Freund&amp;#39;s Adjuvant (CFA) caused intense knee edema reduced by implementing Anti-IL-6, Anti-Fkn and Inh-NF-ĸB. The results indicated elevated levels of apoptotic markers during the acute phase, along with an increase in IL-6, NF-ĸB and Fkn. Although IL-6, NF-ĸB and Fkn levels elevation continued during chronic phase, the apoptosis markers decreased in this phase. The findings revealed that Anti-IL-6 treatment during different phases of study can change the synovial NF-ĸB and Fkn.&lt;br&gt;
&lt;strong&gt;Conclusion:&lt;/strong&gt; It seems that time-dependent variations in apoptotic markers level may be involved in pathogenesis of Adjuvant-induced knee arthritis. In conclusion, synovial IL-6 through NF-ĸB- Fkn pathway can play an important role in this process.&lt;br&gt;
&lt;strong&gt;Keywords:&lt;/strong&gt; Apoptosis, Adjuvant, Fractalkine, IL-6, Inflammation, NF-ĸB&lt;br&gt;
&amp;nbsp;</abstract>
	<keyword_fa></keyword_fa>
	<keyword>Apoptosis, Adjuvant, Fractalkine, IL-6, Inflammation, NF-ĸB</keyword>
	<start_page>168</start_page>
	<end_page>177</end_page>
	<web_url>http://mjiri.iums.ac.ir/browse.php?a_code=A-10-4636-1&amp;slc_lang=en&amp;sid=1</web_url>


<author_list>
	<author>
	<first_name>Sahar </first_name>
	<middle_name></middle_name>
	<last_name>Golabi</last_name>
	<suffix></suffix>
	<first_name_fa></first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa></last_name_fa>
	<suffix_fa></suffix_fa>
	<email>sgolabister@gmail.com</email>
	<code>200319475328460063834</code>
	<orcid>200319475328460063834</orcid>
	<coreauthor>No</coreauthor>
	<affiliation>Physiology Department, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, &amp; Abadan Faculty of Medical Sciences, Abadan, Iran</affiliation>
	<affiliation_fa></affiliation_fa>
	 </author>


	<author>
	<first_name>Jalal </first_name>
	<middle_name></middle_name>
	<last_name>Zaringhalam</last_name>
	<suffix></suffix>
	<first_name_fa></first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa></last_name_fa>
	<suffix_fa></suffix_fa>
	<email>jzaringhalam@sbmu.ac.ir</email>
	<code>200319475328460063835</code>
	<orcid>200319475328460063835</orcid>
	<coreauthor>Yes
</coreauthor>
	<affiliation>Physiology Department, School of Medicine, &amp; Neurophysiology Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran </affiliation>
	<affiliation_fa></affiliation_fa>
	 </author>


	<author>
	<first_name>Homa</first_name>
	<middle_name></middle_name>
	<last_name>Manaheji</last_name>
	<suffix></suffix>
	<first_name_fa></first_name_fa>
	<middle_name_fa></middle_name_fa>
	<last_name_fa></last_name_fa>
	<suffix_fa></suffix_fa>
	<email>hshardimanaheji@yahoo.com</email>
	<code>200319475328460063836</code>
	<orcid>200319475328460063836</orcid>
	<coreauthor>No</coreauthor>
	<affiliation>Physiology Department, School of Medicine, &amp; Neurophysiology Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran </affiliation>
	<affiliation_fa></affiliation_fa>
	 </author>


</author_list>


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