Despite they confer important clinical benefits across multiple indications, their use is associated with a wide array of adverse events involving different organs and systems (i.e., liver, kidney, cardiovascular system, skin, and gut). Non-steroidal anti-inflammatory drugs (NSAIDs) represent one of the most widely used classes of drugs ( McGettigan and Henry, 2013). In conclusion, rifaximin prevents diclofenac-induced enteropathy through both anti-bacterial and anti-inflammatory activities. In conclusion, diclofenac induced ileal mucosal lesions, driving inflammatory pathways and microbiota changes. In LPS-primed THP-1 cells stimulated by nigericin (a model to study the NLRP3 inflammasome), rifaximin reduced IL-1β production in a concentration-dependent fashion, this effect being associated with inhibition of the up-stream caspase-1 activation. This drug was also capable of increasing the proportion of Lactobacilli, a genus depleted by the NSAID.
All these changes were counterbalanced by rifaximin co-administration. In addition, the NSAID decreased ileal occludin expression and provoked a shift of bacterial phyla toward an increase in Proteobacteria and Bacteroidetes abundance. Diclofenac induced intestinal damage and inflammation, triggering an increase in tissue concentrations of tumor necrosis factor and interleukin-1β, higher expression of TLR-2 and TLR-4, MyD88, NF-κB and activation of caspase-1. In addition, the modulating effect of rifaximin on NLRP3 inflammasome was tested in an in vitro cell system. At the end of treatments, parameters dealing with ileal damage, inflammation, barrier integrity, microbiota composition, and TLR-NF-κB-inflammasome pathway were evaluated.
Rifaximin (delayed release formulation) was administered (50 mg/kg BID) 1 h before the NSAID. Enteropathy was induced in 40-week old male rats by intragastric diclofenac (4 mg/kg BID, 14 days). This study examined the pathophysiology of NSAID-associated intestinal lesions in a rat model of diclofenac-enteropathy and evaluated the effect of rifaximin on small bowel damage. Non-steroidal anti-inflammatory drugs (NSAIDs) can damage the small intestine, mainly through an involvement of enteric bacteria. 6Clinical Pharmacology & Digestive Pathophysiology Unit, Department of Clinical & Experimental Medicine, University of Parma, Parma, Italy.5Manchester Collaborative Centre for Inflammation Research, University of Manchester, Manchester, United Kingdom.4Department of Translational Research and New Technologies in Medicine and Surgery, University of Pisa, Pisa, Italy.3Reasearch & Development Department, Alfasigma SpA, Bologna, Italy.2Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy.1Department of Pharmaceutical and Pharmacological Sciences, University of Padua, Padua, Italy.
Since 1986, engineers around the world have been using Synopsys technology to design and create billions of chips and systems.Rocchina Colucci 1, Carolina Pellegrini 2, Matteo Fornai 2, Erika Tirotta 2, Luca Antonioli 2, Cecilia Renzulli 3, Emilia Ghelardi 4, Elena Piccoli 4, Daniela Gentile 2, Laura Benvenuti 2, Gianfranco Natale 4, Federica Fulceri 4, Pablo Palazón-Riquelme 5, Gloria López-Castejón 5, Corrado Blandizzi 2 and Carmelo Scarpignato 6* As a leader in electronic design automation (EDA) and semiconductor IP, Synopsys delivers software, IP and services to help engineers address their design, verification, system and manufacturing challenges. accelerates innovation in the global electronics market.
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Synopsys, Inc., a world leader in software and IP used in the design, verification and manufacture of electronic components and systems, has released K-2015.09 version of Synplify, is provides a high-quality, high-performance, and easy-to-use FPGA implementation and debug environment.ĭesigners using Synopsys’ FPGA tool suite gain fast time-to-results for complex FPGAs, area optimization for both cost and power reduction, automation for soft error mitigation, hierarchical design capabilities and multi-FPGA vendor support.
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