Marcos F F Calabresi1, Alexandre Tanimoto2, André G Próspero3, Fabio P F Mello4, Guilherme Soares4, Luiz C Di Stasi5, José R A Miranda6. 1. Laboratory of Biomagnetism, Department of Physics and Biophysics, Bioscience Institute, São Paulo State University, Botucatu, São Paulo, Brazil. Electronic address: mfcalabresi@ibb.unesp.br. 2. Laboratory of Phytomedicines, Pharmacology and Biotechnology, Department of Pharmacology, Bioscience Institute, São Paulo State University, Botucatu, São Paulo, Brazil. Electronic address: alexandre.tanimoto@unesp.br. 3. Laboratory of Biomagnetism, Department of Physics and Biophysics, Bioscience Institute, São Paulo State University, Botucatu, São Paulo, Brazil. Electronic address: agprospero@ibb.unesp.br. 4. Laboratory of Biomagnetism, Department of Physics and Biophysics, Bioscience Institute, São Paulo State University, Botucatu, São Paulo, Brazil. 5. Laboratory of Phytomedicines, Pharmacology and Biotechnology, Department of Pharmacology, Bioscience Institute, São Paulo State University, Botucatu, São Paulo, Brazil. Electronic address: ldistasi@ibb.unesp.br. 6. Laboratory of Biomagnetism, Department of Physics and Biophysics, Bioscience Institute, São Paulo State University, Botucatu, São Paulo, Brazil. Electronic address: jmiranda@ibb.unesp.br.
Abstract
AIMS: Inflammatory bowel disease is a chronic relapsing inflammation that affects the gastrointestinal tract, causing changes in colonic motility. The evolution of these changes is not completely understood and possibly related to symptoms that appear in different degrees of the intestinal inflammation. Therefore, our aim is evaluate during 14 days of assessment aspects of colonic contractility using 2,4,6-trinitrobenzenesulfonic acid (TNBS) model of inflammation in rats and associate the inflammatory process with colonic motility. METHODS: Contractility and inflammatory parameters were assessed in the same animal in six different moments: before intestinal inflammation induction, 2, 5, 8, 11, and 14 days after induction. The mechanical activity was determined by alternating current biosusceptometry (ACB) and subdivided into rhythmic propagating ripples (RPR) and rhythmic propulsive motor complexes (RPMC). We assessed inflammation by determining myeloperoxidase activity in feces. RESULTS: Transient and permanent changes were observed in colonic motility as a function of the inflammatory process evaluated through myeloperoxidase activity. We identified two contraction profiles: RPR and RPMC. The microscopic analysis demonstrated a depth of damage caused by an injury that was associated with changes in motility. CONCLUSIONS: We implemented a robust and adequate (specific) signal processing to quantify two measured colonic frequency patterns. Thus, we performed a detailed temporal analysis of the consequences of TNBS-induced inflammation on colonic motility in rats. Our approach enables further long-term assessments in the same animal with different mechanisms and duration of injury, remission, treatments and their motor consequences.
AIMS: Inflammatory bowel disease is a chronic relapsing inflammation that affects the gastrointestinal tract, causing changes in colonic motility. The evolution of these changes is not completely understood and possibly related to symptoms that appear in different degrees of the intestinal inflammation. Therefore, our aim is evaluate during 14 days of assessment aspects of colonic contractility using 2,4,6-trinitrobenzenesulfonic acid (TNBS) model of inflammation in rats and associate the inflammatory process with colonic motility. METHODS: Contractility and inflammatory parameters were assessed in the same animal in six different moments: before intestinal inflammation induction, 2, 5, 8, 11, and 14 days after induction. The mechanical activity was determined by alternating current biosusceptometry (ACB) and subdivided into rhythmic propagating ripples (RPR) and rhythmic propulsive motor complexes (RPMC). We assessed inflammation by determining myeloperoxidase activity in feces. RESULTS: Transient and permanent changes were observed in colonic motility as a function of the inflammatory process evaluated through myeloperoxidase activity. We identified two contraction profiles: RPR and RPMC. The microscopic analysis demonstrated a depth of damage caused by an injury that was associated with changes in motility. CONCLUSIONS: We implemented a robust and adequate (specific) signal processing to quantify two measured colonic frequency patterns. Thus, we performed a detailed temporal analysis of the consequences of TNBS-induced inflammation on colonic motility in rats. Our approach enables further long-term assessments in the same animal with different mechanisms and duration of injury, remission, treatments and their motor consequences.
Authors: Guilherme Soares; Leonardo Pinto; Maik Liebl; Gabriel Biasotti; Andre Prospero; Erick Stoppa; Andris Bakuzis; Oswaldo Baffa; Frank Wiekhorst; José Ricardo Arruda Miranda Journal: J Biol Eng Date: 2022-10-11 Impact factor: 6.248