Guilherme Antônio Lopes de Oliveira1, Catalina Alarcón de la Lastra2, Maria Ángeles Rosillo2, Maria Luisa Castejon Martinez2, Marina Sánchez-Hidalgo2, Jand Venes Rolim Medeiros3, Isabel Villegas4. 1. Postgraduate Program in Biotechnology, Northeast Biotechnology Network (RENORBIO) Federal University of Piauí, São Sebastião Street 2819, 64202-020, Parnaíba, PI, Brazil. 2. Department of Pharmacology, Faculty of Pharmacy, University of Seville, Profesor García González Street 2, 41012, Seville, Spain. 3. Postgraduate Program in Biotechnology, Northeast Biotechnology Network (RENORBIO) Federal University of Piauí, São Sebastião Street 2819, 64202-020, Parnaíba, PI, Brazil. Electronic address: jandvenes@ufpi.edu.br. 4. Department of Pharmacology, Faculty of Pharmacy, University of Seville, Profesor García González Street 2, 41012, Seville, Spain. Electronic address: villegas@us.es.
Abstract
Ulcerative colitis is an idiopathic inflammatory bowel disease characterized by intestinal inflammation; blocking this inflammatory process may be the key to the development of new naturally occurring anti-inflammatory drugs, with greater efficiency and lower side effects. The objective of this study is to explore the effects of bergenin (BG) in TNBS (2,4,6-trinitrobenzenesulfonic acid)-induced acute colitis model in rats in order to assist in the studies for the development of novel natural product therapies for inflammatory bowel disease. 48 Wistar rats were randomized into six groups: (i) Control and (ii) TNBS control; (iii) 5-ASA 100 mg/kg/day (iv) BG 12 mg/kg/day (v) BG 25 mg/kg/day and (vi) BG 50 mg/kg/day. Colitis was induced by instillation of TNBS. Colitis was evaluated by an independent observer who was blinded to the treatment. Our results revealed that bergenin decreased the macroscopic and microscopic damage signs of colitis, and reduced the degree of neutrophilic infiltration in the colon tissue; also, it was capable to down-regulate COX-2, iNOS, IkB-α, and pSTAT3 protein expression. Similarly, using a protocol for indirect ELISA quantification of cytokines, bergenin treatment reduced IL-1β, IFN-γ and IL-10 levels, and inhibited both canonical (IL-1) and non-canonical (IL-11) NLRP3/ASC inflammasome signaling pathways in TNBS-induced acute colitis. Conclusion: Our study has provided evidence that administration of bergenin reduced the damage caused by TNBS in an experimental model of acute colitis in rats, reduced levels of pro-inflammatory proteins and cytokines probably by modulation of pSTAT3 and NF-κB signaling and blocking canonical and non-canonical NLRP3/ASC inflammasome pathways.
Ulcerative colitis is an idiopathic inflammatory bowel disease characterized by intestinal inflammation; blocking this inflammatory process may be the key to the development of new naturally occurring anti-inflammatory drugs, with greater efficiency and lower side effects. The objective of this study is to explore the effects of bergenin (BG) in TNBS (2,4,6-trinitrobenzenesulfonic acid)-induced acute colitis model in rats in order to assist in the studies for the development of novel natural product therapies for inflammatory bowel disease. 48 Wistar rats were randomized into six groups: (i) Control and (ii) TNBS control; (iii) 5-ASA 100 mg/kg/day (iv) BG 12 mg/kg/day (v) BG 25 mg/kg/day and (vi) BG 50 mg/kg/day. Colitis was induced by instillation of TNBS. Colitis was evaluated by an independent observer who was blinded to the treatment. Our results revealed that bergenin decreased the macroscopic and microscopic damage signs of colitis, and reduced the degree of neutrophilic infiltration in the colon tissue; also, it was capable to down-regulate COX-2, iNOS, IkB-α, and pSTAT3 protein expression. Similarly, using a protocol for indirect ELISA quantification of cytokines, bergenin treatment reduced IL-1β, IFN-γ and IL-10 levels, and inhibited both canonical (IL-1) and non-canonical (IL-11) NLRP3/ASC inflammasome signaling pathways in TNBS-induced acute colitis. Conclusion: Our study has provided evidence that administration of bergenin reduced the damage caused by TNBS in an experimental model of acute colitis in rats, reduced levels of pro-inflammatory proteins and cytokines probably by modulation of pSTAT3 and NF-κB signaling and blocking canonical and non-canonical NLRP3/ASC inflammasome pathways.
Authors: Tamara Ortiz; Federico Argüelles-Arias; Matilde Illanes; Josefa-María García-Montes; Elena Talero; Laura Macías-García; Ana Alcudia; Victoria Vázquez-Román; Virginia Motilva; Manuel De-Miguel Journal: Nutrients Date: 2020-06-11 Impact factor: 5.717
Authors: Cristiane F Villarreal; Dourivaldo S Santos; Pedro S S Lauria; Kelly B Gama; Renan F Espírito-Santo; Paulo J L Juiz; Clayton Q Alves; Jorge M David; Milena B P Soares Journal: Int J Mol Sci Date: 2020-07-09 Impact factor: 5.923