EXCLI Journal https://www.excli.de/index.php/excli <center><img class="img-responsive" src="/public/site/images/lindemann/Lucida_logo_neu_geschrieben.PNG" alt="EXCLI Journal Logo"></center> <p>EXCLI Journal publishes original research reports, authoritative reviews and case reports of experimental and clinical sciences.</p> <div class="toggleBox"><input id="toggleContent" name="toggleContent" type="checkbox"> <label class="open" for="toggleContent">More...</label> <label class="close" for="toggleContent">Less...</label> <div> <p><strong>EXCLI Journal </strong>(eISSN 1611-2156)&nbsp;is particularly keen to keep a broad view of science and technology, and therefore welcomes papers which bridge disciplines and may not suit the narrow specialism of other journals. Although the general emphasis is on biological sciences, studies from the following fields are explicitly encouraged:</p> <p>Immunology, toxicology, ergonomics, neurosciences, psychology, occupational medicine, clinical and preclinical studies, drug development, pharmacology, environmental health, chemistry including analytical chemistry, biochemistry, cell biology, genetics, forensic medicine, oncology and cancer research, proteomics, systems biology, hepatology and gastroenterology, aging research, psychiatric research, behavioral sciences.</p> </div> </div> en-US <p>Authors who publish in this journal agree to the following terms:</p> <ul> <li>The authors keep the copyright and grant the journal the right of first publication under the terms of the Creative Commons Attribution license, <a href="https://creativecommons.org/licenses/by/4.0/" target="_blank" rel="noopener">CC BY 4.0</a>. This licencse permits unrestricted use, distribution and reproduction in any medium, provided that the original work is properly cited.</li> <li>The use of general descriptive names, trade names, trademarks, and so forth in this publication, even if not specifically identified, does not imply that these names are not protected by the relevant laws and regulations.</li> <li>Because the advice and information in this journal are believed to be true and accurate at the time of publication, neither the authors, the editors, nor the publisher accept any legal responsibility for any errors or omissions presented in the publication. The publisher makes no guarantee, express or implied, with respect to the material contained herein.</li> <li>The authors can enter into additional contracts for the non-exclusive distribution of the journal's published version by citing the initial publication in this journal (e.g. publishing in an institutional repository or in a book).</li> </ul> excli@ifado.de (EXCLI Journal) excli@ifado.de (Webmaster) Mon, 04 Jan 2021 08:22:24 +0100 OJS 3.2.1.1 http://blogs.law.harvard.edu/tech/rss 60 Review article: The Molecular Mechanisms of Curcumin Action in Experimental Autoimmune Encephalomyelitis, A Model of Multiple Sclerosis https://www.excli.de/index.php/excli/article/view/3771 <p>Multiple sclerosis (MS) is an autoimmune inflammatory disorder of the central nervous system (CNS) that leads to demyelination and degeneration of neurons. Several different animal models have been developed to study MS disease. Immunization of host animals (e.g. mice or rats) with autoantigen proteins combined with adjuvant or transfer of activated CD4<sup>+ </sup>myelin-specific T lymphocytes to the hosts are two protocols for inducing experimental autoimmune encephalomyelitis (EAE) which are commonly used in these investigations. Curcumin has shown several beneficial effects in experimental studies including anti-oxidative, anti-proliferative and anti-inflammatory functions.. In addition, it is commonly used in traditional medicine to treat inflammation and promote wound healing. This nutrient can alleviate the EAE mice symptoms and downregulate neural antigen-specific T helper (Th)1 and Th17 cell differentiation. Moreover, curcumin through directly acts on T cells and indirectly attenuates interleukin (IL)-12 and IL-23 production. It can regulate the Th1/Th17 responses in EAE mice and can improve the severity of symptoms in the spinal cord injury (SCI) model by modulating the mammalian target of rapamycin (mTOR) Pathway signaling. Curcumin enhances neurotrophic factors and repairs mechanisms in CNS via rebuild of the myelin. Therefore, curcumin can down-regulate the progression of MS disease. In present review, all original articles were searched from international databases including Medline (PubMed), Google Scholar, Scopus, and CINHAL. We arranged a systematic review of relevant papers published in English between January 1980 to January 2021. The suitable keywords indexed in the Medical Subject Heading (MeSH) or Embase, and the following search phrases were searched: Multiple Sclerosis, autoimmune encephalomyelitis and curcumin.</p> Behrouz Robat-Jazi, Ali Akbar Saboor-Yaraghi Copyright (c) https://www.excli.de/index.php/excli/article/view/3771 Topical phenytoin accelerates the healing of acetic acid-induced colitis in Rats: evaluating of Transforming growth factor-beta, Platelet-derived growth factor, and Vascular endothelial growth factor. https://www.excli.de/index.php/excli/article/view/3768 <p>BACKGROUND: Ulcerative colitis (UC) limited to the innermost lining of the colon has become a global health problem. Immunomodulatory and monoclonal antibodies are using despite their side effects and limitations of effective choices. Phenytoin is using to heal wounds due to its side effects like the increased expression of growth factors, collagen, and extracellular matrix synthesis.</p> <p>OBJECTIVE: This study aimed to evaluate the effect of topical phenytoin in UC.</p> <p>DESIGN: Phenytoin in two-doses and period treatment had investigated.</p> <p>SETTINGS: Male Wistar rats (230–280 g, n=8) were divided randomly into ten groups.</p> <p>PATIENTS: This study didn't use the human-related protocol.</p> <p>INTERVENTIONS: Animals divided as follows: Sham, control, hydrocortisone, phenytoin 1%, and 3% groups in six or 12-days treatment protocol. Ulcerative colitis model was induced by administration acetic acid 4% into the colon transracially animals were sacrificed at postoperative days 7 and 13.</p> <p>MAIN OUTCOME MEASURES: Bodyweight loss, Microscopic score, and Ulcer index measured using specific criteria, and growth factors were measure by western blotting.</p> <p>RESULTS: Bodyweight loss reversed in treatment groups. Ulcer index in six and 12-day had reduced. Microscopic score in six-day enema treatment significantly decreased in treatment groups compared to the control groups. TGF-β in a time-dependent and PDGF and VEGF time and dose-dependently in phenytoin 1% and3% significantly increased in six and 12-day protocol.</p> <p>LIMITATIONS: Acetic acid-induced UC in rats may not be matched wholly with the development and process of UC in humans.</p> <p>CONCLUSIONS: Phenytoin dose and time-dependently reversed weight loss. Also, histopathological parameters include microscopic scores, and ulcer index was decreased via the induction of growth factors TGF-β, PDGF, and VEGF and accelerate ulcer healing.</p> Nima Fattahi, Alina Abdolahi, Zakarya Vahabzadeh, Bahram Nikkhoo, Farhad Manoochehri, Sara Goudarzzadeh, Kambiz Hassanzadeh, Esmaeil Izadpanah, Mohammad Raman Moloudi Copyright (c) https://www.excli.de/index.php/excli/article/view/3768 Lungs epithelial cells injury induced by C-reactive protein (CRP) is mediated via p38 MAPK/mitochondrial apoptosis pathway https://www.excli.de/index.php/excli/article/view/3770 <p>Increased level of C-reactive protein (CRP) are known to be associated with <em>Mycoplasma pneumoniae</em> (MP) infection. The purpose of this study was to explore whether C-reactive protein (CRP) causes the apoptosis of lung epithelial cells after MP infection and the underlying mechanism. <em>M. pneumoniae</em> pneumonia (MPP) patients were included for CRP detection using immuno-turbidimetry and western blot. The expression of CRP in A549 cells was detected by immuno-fluorescence, qRT-PCR, western blot and immunoturbidimetric. The viability of A549 cells was detected by MTT, the expressions of p38 MAPK/mitochondrial apoptotic pathway-related proteins were evaluated by western blot, and the apoptosis was determined by flow cytometry. The expressions of Cyt C and Tom 20 were observed by immuno-fluorescence, the mitochondrial membrane potential (ΔΨm) was detected by JC-1, and ROS content was measured by DCFH-DA. We found that the expression of CRP was elevated in blood of MPP patients. The expression of CRP in MP-infected A549 cells increased significantly. The cell viability was significantly reduced, the cell morphology was abnormal and the rate of apoptosis was markedly increased in MP group. Next, overexpression of CRP induced the up-regulation of the p38 MAPK/mitochondrial apoptosis pathway related protein expression levels and increased Cyt C expression in the cytoplasm, decreased Tom 20 expression and ΔΨm and up-regulated ROS expression. The addition of SB203580 and CsA alleviated the damage of CRP to A549 cells. The increased CRP induced by MP infection, caused apoptosis of lung epithelial cells through the p38 MAPK/mitochondrial apoptosis pathway.</p> Liping Yu, Dr, Dr Copyright (c) https://www.excli.de/index.php/excli/article/view/3770