Cristiano Trindade de Andrade1, Guilherme Zweig Rocha1, Marina Zamuner1, Rodolfo Borges Dos Reis2, Leonardo Oliveira Reis3,1. 1. UroScience, Urology Division, Department of Surgery, State University of Campinas (UNICAMP) Campinas, SP, Brazil. 2. Urology Division, Department of Surgery, University of Ribeirão Preto, USP-RP SP, Brazil. 3. Urology Division, Center for Life Sciences, Pontifical Catholic University of Campinas (PUC-Campinas) Campinas, SP, Brazil.
Abstract
BACKGROUND: Recently, the role of subclinical inflammation in obesity has gained prominence. An association between obesity and chronic inflammation has been observed in several studies that show a relationship between increased morbidity and high Body Mass Index (BMI). This study aims to compare inflammatory pathways in obese (by high-fat diet) and non-obese mice after exposure to an intravesical carcinogen in a cystitis model. METHODS: We divided 16 female, 7 week old mice into two groups: 1) CONTROL: standard diet, and 2) OBESE: high fat diet for 8 weeks. Both groups underwent a protocol for N-Nitroso-N-methylurea (MNU) pro-inflammatory bladder instillation. Bladder was analyzed by histopathology and western blotting for proteins of the inflammatory pathway (JNK, NFκB, c-JUN, IKK), and immunohistochemistry (proliferation and apoptosis). RESULTS: While mice eating standard diet showed minimal histologic alteration in 4 of 5 (80%) bladder tissues, those eating a high fat diet showed moderate (60%) and intense (40%) chronic active inflammation with dysplasia foci, increased proliferation, apoptosis and inflammatory pathway activation with increased NFκB, and also IKKβ, JNK, and c-JUN phosphorylation in the urothelium. CONCLUSION: A high-fat diet causes increased urothelial proliferation, apoptosis, and NFκB expression with cystitis exacerbation and dysplasia. Together, these results suggest that obesity induced by a high-fat diet increases the inflammatory pathway in the bladder with possible pre-malignant alterations. IJCEP
BACKGROUND: Recently, the role of subclinical inflammation in obesity has gained prominence. An association between obesity and chronic inflammation has been observed in several studies that show a relationship between increased morbidity and high Body Mass Index (BMI). This study aims to compare inflammatory pathways in obese (by high-fat diet) and non-obese mice after exposure to an intravesical carcinogen in a cystitis model. METHODS: We divided 16 female, 7 week old mice into two groups: 1) CONTROL: standard diet, and 2) OBESE: high fat diet for 8 weeks. Both groups underwent a protocol for N-Nitroso-N-methylurea (MNU) pro-inflammatory bladder instillation. Bladder was analyzed by histopathology and western blotting for proteins of the inflammatory pathway (JNK, NFκB, c-JUN, IKK), and immunohistochemistry (proliferation and apoptosis). RESULTS: While mice eating standard diet showed minimal histologic alteration in 4 of 5 (80%) bladder tissues, those eating a high fat diet showed moderate (60%) and intense (40%) chronic active inflammation with dysplasia foci, increased proliferation, apoptosis and inflammatory pathway activation with increased NFκB, and also IKKβ, JNK, and c-JUN phosphorylation in the urothelium. CONCLUSION: A high-fat diet causes increased urothelial proliferation, apoptosis, and NFκB expression with cystitis exacerbation and dysplasia. Together, these results suggest that obesity induced by a high-fat diet increases the inflammatory pathway in the bladder with possible pre-malignant alterations. IJCEP
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