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Excised rat intestinal tissue mounted in an Ussing chamber can be used for intestinal permeability assessments in drug development. The outer layer of the intestine, the serosa and part of the muscle layer, is traditionally removed since it is considered a barrier to the diffusion of nutrients and oxygen as well as to that of pharmaceutical substances. However, the procedure for removing the serosal-muscle layer, i.e. stripping, is a technically challenging process in the pre-experimental preparation of the tissue which may result in tissue damage and reduced viability of the segment. In this study, the viability of stripped and native (non-stripped) rat small intestine tissue segments mounted in Ussing chambers was monitored and the apparent permeability of the tissue to a set of test compounds across both tissue preparations was determined. Electrical measurements, in particular the potential difference (PD) across the intestinal membrane, were used to evaluate the viability. In this study, there were no differences in initial PD (health status of the tissue) or PD over time (viability throughout the experiment) between native and stripped rat jejunum segments. Overall, there were also no significant differences in permeability between stripped and native rat intestinal tissue for the compounds in this study. Based on these results, we propose that stripping can be excluded from the preparation procedures for rat jejunal tissue for permeability studies when using the Ussing chamber technique.
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http://dx.doi.org/10.1016/j.ijpharm.2016.03.063 | DOI Listing |
J Anim Sci
August 2025
Department of Animal Sciences, University of Illinois Urbana-Champaign, Urbana, IL, USA, 61801.
The objective was to determine the effects of induced hindgut acidosis in sheep on cecal pH, ruminal fermentation, and gut permeability. Eleven ruminally and cecally cannulated ewes (49 ± 4 kg) were assigned to one of two treatments: control (CON; n = 5) or induced hindgut acidosis (HGA; n = 6). To induce hindgut acidosis, 3 g wheat starch/kg BW per 24 h was continuously infused via the cecal cannula for 4 d.
View Article and Find Full Text PDFFront Pharmacol
August 2025
Department of Radiation Oncology, University of Florida, Gainesville, FL, United States.
Introduction: In cystic fibrosis (CF), most CFTR mutations cause partial (Class II) or complete (Class I) loss of function. Modulators (VX) can improve CFTR function in Class II mutations but are ineffective for Class I mutations and may cause side effects, resulting in tolerability issues with concerns about long-term safety. Apical anion secretion, essential for maintaining airway surface liquid (ASL) homeostasis, is regulated by CFTR.
View Article and Find Full Text PDFGut Microbes
December 2025
Nutrition-Gut-Brain Interactions Research Centre, School of Medical Sciences, Faculty of Medicine and Health, Örebro University, Örebro, Sweden.
Irritable bowel syndrome (IBS) is a prevalent gastrointestinal disorder for which effective treatment strategies are insufficient. Butyrate, a microbiota-derived short-chain fatty acid believed to strengthen the intestinal barrier function, might be a potential new treatment option. This study aimed to investigate potential protective effects of acute butyrate exposure on intestinal barrier function in healthy subjects and patients with IBS.
View Article and Find Full Text PDFInt J Mol Sci
August 2025
Department of General Pediatrics, University Hospital Muenster, Albert-Schweitzer-Campus 1, 48149 Muenster, Germany.
Cystic fibrosis (CF), the most common hereditary lung disease in Caucasians, is caused by dysfunction of the cystic fibrosis transmembrane conductance regulator (CFTR). We evaluated CFTR function using a newly developed Ussing chamber system, the Multi Trans Epithelial Current Clamp (MTECC), in an in vitro model of human airway epithelia. Air-liquid interface (ALI) cultures were established from nasal brushings of healthy controls (HC) and CF patients with biallelic CFTR variants.
View Article and Find Full Text PDFAm J Physiol Lung Cell Mol Physiol
August 2025
Laboratoire de physiopathologie et régulation des transports ioniques, Pôle Biologie Santé, Université de Poitiers, 86073 Poitiers, France.
Trikafta (elexacaftor/tezacaftor/ivacaftor, ETI) is approved for cystic fibrosis (CF) patients with at least one F508del mutation in the CFTR gene or another responsive mutation based on data. However, the pharmacological effects of ETI on F508del-CFTR remain incompletely defined in vitro. To explore the mechanisms underlying Trikafta's clinical efficacy, we used primary bronchial epithelial cells from F508del homozygous patients and CFBE41o- cells expressing F508del-CFTR.
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