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) Thu, 02 Jan 2020 09:10:20 +0100 OJS 3.2.1.1 http://blogs.law.harvard.edu/tech/rss 60 Copper Oxide Nanoparticles Promote α-Synuclein Fibrillation and Underlying Neurotoxicity as A Model of Parkinson Disease https://www.excli.de/index.php/excli/article/view/2781 <p>Parkinson's disease is associated with the formation of protein aggregates called amyloid fibrils. α-Synuclein amyloid accumulation is known to be a key factor in the development of neuronal degenerative diseases in the brain, and exploring some toxic compounds with biomedical application like copper oxide (CuO) nanoparticles that can promote aggregation or toxicity are the focus of preventive care studies on Parkinson's disease. Hence, in this study, the effects of synthesized CuO nanoparticles by sol-gel method on the promoting neuronal toxicity of α-synuclein aggregated species was investigated. For this purpose, the fabricated Cuo nanoparticles were characterized by SEM and TEM techniques. Afterwards, the process of α-synuclein fibrillation was induced and standardized approaches such as fluorescence and circular dichroism spectroscopy as well as TEM approach were used. The toxicity of α-synuclein fibrils either alone or co-incubated with CuO nanoparticles was then assessed against SH-SY5Y cells using different methods such as MTT, LDH, caspase-3 and qPCR assays. It was observed that spherical-shaped synthesized nanoparticles provide a diameter of about 50 nm. ThT fluorescence, Congo red, circular dichroism and TEM studies showed that CuO nanoparticles promote the fibrillation process of α-synuclein. Also, cellular and molecular assays showed that the relative cytotoxicity of α-synuclein amyloid fibrils co-incubated with CuO nanoparticles is more significant than α-synuclein amyloid alone. In conclusion, it can be suggested that CuO nanoparticles increase the detrimental effects of α-synuclein toxic aggregates and can be considered to promote the transmission and spread of α-synuclein aggregation-related toxicity.</p> Qingzhi Li Copyright (c) https://www.excli.de/index.php/excli/article/view/2781 FIBROBLAST GROWTH FACTOR 21 ATTENUATES OXIDATIVE STRESS, INFLAMMATION AND APOPTOSIS INDUCED BY H2O2 IN MODE-K CELLS https://www.excli.de/index.php/excli/article/view/2780 <p>Oxidative stress is associated with many intestinal diseases. FGF-21 has been considered to regulate oxidative stress in metabolic diseases. However, the effect of FGF-21 on intestinal oxidative stress and its mechanism has not fully understood. Therefore, in this study, we used H2O2 to induce oxidative stress in MODE-K cells and cells were preincubated with or without FGF-21. Determination of redox status was to detect the level of ROS, MDA and GSH and the activity of SOD, CAT, GSH-Px and T-AOC. Cell viability and cell apoptosis were detect by MTT test and Annexin V-FITC/PI Staining. Inflammatory state was measured by ELISA and real-time PCR. Western blotting was to detect the signaling pathway. Our results showed that FGF-21 significantly improved redox status through increasing the GSH level and the activity of SOD, CAT, GSH-Px and T-AOC and decreasing the level of ROS and MDA in H2O2-induced MODE-K cells. Besides, FGF-21 reduced cell apoptosis by decreasing the expressions of Bax and Caspase 3. Moreover, FGF-21 reduced inflammatory factors including IL-1β, IL-6, IL-8 and TNF-α expression. Furthermore, FGF-21 exerted its anti-oxidative and anti-inflammatory effects via activating Nrf2 signaling pathway and inhibiting NF-κB signaling pathway in H2O2-induced MODE-K cells. In conclusion, FGF-21 attenuates oxidative stress, inflammation and apoptosis induced by H2O2 in MODE-K cells and may show multiple beneficial effects on oxidative stress related diseases.</p> Nan Wang, Xing Kang, Shuai Li, Xiao-chen Guo, Wen-fei Wang, De-shan Li Copyright (c) https://www.excli.de/index.php/excli/article/view/2780 ANDROGEN RECEPTOR SPLICE VARIANTS AR-V7 AND AR-V567ES PROMOTE PROSTATE CANCER METASTASIS BY MODULATING EXPRESSION OF POTENTIAL REGULATORY SIGNALING MOLECULES https://www.excli.de/index.php/excli/article/view/2778 <p>Androgen receptor splice variants (AR-Vs) produced by alternative splicing of the AR play an important role in the treatment resistance and progression of prostate cancer (PCa). In this study, two most common AR variants and how they associate with the inflammatory response (NF-Kβ) and regulatory transcriptional activity (HSP-27) genes were investigated in patients with PCa and metastatic PCa (Met-PCa). Our study was carried out with the whole blood obtained from 25 healthy control subjects, 25 PCa patients and 39 Met-PCa patients. We examined the expression levels of AR, AR-V7 and AR-V567es genes via Real-time PCR and those of HSP-27 and NF-Kβ via ELISA method. AR, AR-V7 and AR-V567es expressions were observed in 84.61%, 64.1%, 23.07% of Met-PCa patients respectively. The expression levels of full-length AR and variants (AR-V7 and AR-V567es) were associated with the prostate cancer stage. In the Met-PCa, the expression levels of AR, AR-V7 and AR-V567es were associated with the Gleason Scores but not with the PSA levels. AR-V7 expression levels in stage T4 patients significantly increased.NF-Kβ and HSP-27 protein levels were significantly higher in Met-PCa patients. Our findings highlight the targeting of the proteostasis and inflammation pathways through inhibiting HSP-27 and NF-Kβ. This might be a valuable strategy to overcome anti-androgen resistance and improve drug therapy in Met-PCa patients whose gene expression levels of AR-V7 and AR-V567es variants are high.</p> Ilker Kiliccioglu, Cenk Y. Bilen, Sinan Sozen, Ece Konaç Copyright (c) https://www.excli.de/index.php/excli/article/view/2778