International Journal of Preventive Medicine (Int J Prev Med)2008-7802142017091118251825ENDepartment of Physiology, School of Medicine, Mashhad University of Medical Sciences, MashhadDepartment of Physiology, School of Medicine, Esfarayen Faculty of Medical Sciences, EsfarayenDepartment of Physiology, School of Medicine, Mashhad University of Medical Sciences, MashhadDepartment of Physiology, School of Medicine, Mashhad University of Medical Sciences, MashhadNeurocognitive Research Center, School of Medicine, Mashhad University of Medical Sciences, Mashhad,Department of Pathology, School of Medicine, Mashhad University of Medical Sciences, MashhadNeurogenic Inflammation Research Center, School of Medicine, Mashhad University of Medical Sciences, Mashhad20170911<p><span class="fontstyle0"><strong>Background</strong>: </span><span class="fontstyle2">Renin‑angiotensin (Ang)‑aldosterone system not only plays a key role in the regulation of circulatory homeostasis, but also it acts as a powerful pro‑inflammatory mediator. The aim of this study was to evaluate the effect of captopril (Cap), a known Ang‑converting enzyme inhibitor, on inflammation‑induced cardiac fbrosis, and heart oxidative stress status in<br />lipopolysaccharide (LPS)‑induced inflammation in male rats. </span></p><p><strong></strong><span class="fontstyle0"><strong>Methods</strong>: </span><span class="fontstyle2">Fifty male rats were randomly divided into fve groups control, LPS (1 mg/kg/day), LPS + Cap 10 mg/kg, LPS + Cap 50 mg/kg and LPS + Cap 100 mg/kg. After 2 weeks, blood samples were taken, and hearts were harvested for evaluation of tumor necrosis factor alpha (TNF‑</span><span class="fontstyle3">&alpha;</span><span class="fontstyle2">), interleukin‑6 (IL‑6) and nitric oxide metabolite in serum and tissue hemogenate, histopathology (hematoxylin and eosin and Masson&rsquo;s<br />trichrome) and oxidative stress status. </span></p><p><strong></strong><span class="fontstyle0"><strong>Results</strong>: </span><span class="fontstyle2">Serum IL‑6 and TNF‑</span><span class="fontstyle3">&alpha; </span><span class="fontstyle2">concentration were higher in LPS group compared to control and Cap reduced them, signifcantly. Heart TNF‑</span><span class="fontstyle3">&alpha; </span><span class="fontstyle2">and IL‑6 contents in LPS group were signifcantly higher than control (</span><span class="fontstyle4">P </span><span class="fontstyle2">&lt; 0.05). The administration of Cap signifcantly decreased inflammatory markers level to control (</span><span class="fontstyle4">P </span><span class="fontstyle2">&lt; 0.05). The higher levels of malondialdehyde and lower antioxidative markers (total thiol, superoxide dismutase, and catalase)<br />in the heart were observed in LPS group and treatment by Cap improved them, dose‑dependently. Histopathological study revealed cardiac fbrosis and more collagen content in LPS group which signifcantly improved by Cap treatment. </span></p><p><span class="fontstyle0"><strong>Conclusions</strong>: </span><span class="fontstyle2">Treatment by Cap reduced cardiac fbrosis possibly through improving oxidative stress status, and it can be considered to increase cardiac compliance in this condition.<br /></span></p><p><span class="fontstyle0" style="color: #00652e;"><strong>Keywords</strong>: </span><span class="fontstyle4">Angiotensin, cardiac, fbrosis, inflammation</span> <br style="font-style: normal; font-variant: normal; font-weight: normal; letter-spacing: normal; line-height: normal; orphans: 2; text-align: -webkit-auto; text-indent: 0px; text-transform: none; white-space: normal; widows: 2; word-spacing: 0px;" /></p>http://ijpm.mui.ac.ir/index.php/ijpm/article/view/1825http://ijpm.mui.ac.ir/index.php/ijpm/article/download/1825/2112