<?xml version="1.0" encoding="utf-8"?>
<journal>
<title>Reports of Biochemistry and Molecular Biology</title>
<title_fa></title_fa>
<short_title>rbmb.net</short_title>
<subject>Basic Sciences</subject>
<web_url>http://rbmb.net</web_url>
<journal_hbi_system_id>1</journal_hbi_system_id>
<journal_hbi_system_user>admin</journal_hbi_system_user>
<journal_id_issn>2322-3480</journal_id_issn>
<journal_id_issn_online>2322-3480</journal_id_issn_online>
<journal_id_pii></journal_id_pii>
<journal_id_doi>10.61882/rbmb</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>1400</year>
	<month>8</month>
	<day>1</day>
</pubdate>
<pubdate>
	<type>gregorian</type>
	<year>2021</year>
	<month>11</month>
	<day>1</day>
</pubdate>
<volume>10</volume>
<number>3</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>Effect of Nicotine on STAT1 Pathway and Oxidative Stress in Rat Lungs</title>
	<subject_fa>بیوشیمی</subject_fa>
	<subject>Biochemistry</subject>
	<content_type_fa>مقالات اصلی</content_type_fa>
	<content_type>Original Article</content_type>
	<abstract_fa></abstract_fa>
	<abstract>&lt;strong&gt;&lt;em&gt;Background:&lt;/em&gt;&lt;/strong&gt; Tobacco use is responsible for millions of preventable deaths due to cancer. Nicotine, an&amp;nbsp;alkaloid chemical found in tobacco was proved to cause chronic inflammation and oxidative stress. The&amp;nbsp;transcription factor STAT1 induces the expression of many proinflammatory genes and has been suggested&amp;nbsp;to be a target for anti-inflammatory therapeutics. The following study investigated the effect of Nicotine on&amp;nbsp;STAT1 pathway and oxidative stress in rat lung tissue.&amp;nbsp;&lt;br&gt;
&lt;br&gt;
&lt;strong&gt;&lt;em&gt;Methods:&lt;/em&gt;&lt;/strong&gt; Thirty rats were divided into 3 groups; group I considered as control, group II; its rats were&amp;nbsp;daily injected with Nicotine at a dose of 0.4 mg/100 gm body for 8 successive weeks and group III;&amp;nbsp;its rats were daily injected with Nicotine as group II, but the injection was stopped for another 4&lt;br&gt;
weeks. STAT1&amp;alpha; protein was assessed by immunohistochemistry, COX-2 and iNOS genes expression&amp;nbsp;were evaluated by real time PCR and thiobarbituric acid reactive substances (TBARS) and total thiols&amp;nbsp;were measured using spectrophotometric methods in the lung tissues of the rats.&lt;br&gt;
&lt;br&gt;
&lt;strong&gt;&lt;em&gt;Results:&lt;/em&gt;&lt;/strong&gt; The results of the study revealed that group II rats had the highest expression of STAT1&amp;alpha; protein&amp;nbsp;and COX-2 and iNOS genes and oxidative stress in their lung tissues. Nicotine cessation for 4 weeks&amp;nbsp;caused a marked reduction in the expression of STAT1&amp;alpha; protein, COX-2 and iNOS genes and oxidative&amp;nbsp;stress.&lt;br&gt;
&lt;br&gt;
&lt;em&gt;&lt;strong&gt;Conclusions:&lt;/strong&gt;&lt;/em&gt; Induction of STAT1 pathway and the increase in oxidative stress may be the&amp;nbsp;mechanisms through which Nicotine may induce its harmful effects.</abstract>
	<keyword_fa></keyword_fa>
	<keyword>COX-2, iNOS, Nicotine, Oxidative stress, STAT1.</keyword>
	<start_page>429</start_page>
	<end_page>436</end_page>
	<web_url>http://rbmb.net/browse.php?a_code=A-10-469-2&amp;slc_lang=en&amp;sid=1</web_url>


<author_list>
	<author>
	<first_name>Aida Abdeen</first_name>
	<middle_name></middle_name>
	<last_name>Mahmoud</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>aida_mahmoud@med.sohag.edu.eg.</email>
	<code>100319475328460012547</code>
	<orcid>100319475328460012547</orcid>
	<coreauthor>Yes
</coreauthor>
	<affiliation>Department of Medical Biochemistry, Faculty of Medicine, Sohag University, Egypt.</affiliation>
	<affiliation_fa></affiliation_fa>
	 </author>


	<author>
	<first_name>Hekmat</first_name>
	<middle_name></middle_name>
	<last_name>Abdel-Aziz</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></email>
	<code>100319475328460012548</code>
	<orcid>100319475328460012548</orcid>
	<coreauthor>No</coreauthor>
	<affiliation>Department of Medical Histology, Sohag University, Egypt and of</affiliation>
	<affiliation_fa></affiliation_fa>
	 </author>


	<author>
	<first_name>Mohamed</first_name>
	<middle_name></middle_name>
	<last_name>Elbadr</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></email>
	<code>100319475328460012549</code>
	<orcid>100319475328460012549</orcid>
	<coreauthor>No</coreauthor>
	<affiliation>Department of Medical Pharmacology, Faculty of Medicine, Assiut University, Egypt.</affiliation>
	<affiliation_fa></affiliation_fa>
	 </author>


	<author>
	<first_name>Hala</first_name>
	<middle_name></middle_name>
	<last_name>ELBadre</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></email>
	<code>100319475328460012550</code>
	<orcid>100319475328460012550</orcid>
	<coreauthor>No</coreauthor>
	<affiliation>Department of Medical Biochemistry, Faculty of Medicine, Assiut University, Egypt.</affiliation>
	<affiliation_fa></affiliation_fa>
	 </author>


</author_list>


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