title: Obesity promotes oxidative stress and exacerbates sepsis-induced brain damage.
abstract: Sepsis is a severe clinical syndrome in which a system-wide inflammatory response follows initial attempts to eliminate pathogens. It is not novel that in sepsis the brain is one of the first organs affected which causes an increase in morbidity and mortality and its consequences may be exacerbated when associated with a diagnosis of chronic inflammation, such as in obesity. Thus, the aim of the present study is to evaluate the susceptibility to brain damage after sepsis in obese rats. During two months, Wistar rats, 60 days, 250-300g received hypercaloric nutrition to induce obesity. Sepsis was submitted to the cecal ligation and perforation (CLP) procedure and sham-operated rats was considered control group. The experimental groups were divided into Sham + Eutrophic, Sham + Obesity, CLP + Eutrophic and CLP + Obesity. Twelve and twenty four hours after surgery the blood brain barrier (BBB) permeability, nitrite/nitrate concentration, myeloperoxidase (MPO) activity, oxidative damage to lipids and proteins and superoxide dismutase (SOD) and catalase (CAT) activities were evaluated in the hippocampus, cortex and prefrontal cortex. The data indicate that in obese rats subjected to sepsis occurs an increase of BBB permeability in different brain regions compared to eutrophic septic rats. This alteration reflected an increase of MPO activity, concentration of nitrite/nitrate, oxidative damage to lipids and proteins and an imbalance of SOD and CAT especially 24 hours after sepsis. It follows that obesity due to its pro-inflammatory phenotype can aggravate or accelerate the sepsis-induced damage in rat brain.
authors.forename: Andriele Aparecida
authors.initials: AA
authors.lastname: Vieira
authors.forename: Monique
authors.initials: M
authors.lastname: Michels
authors.forename: Drielly
authors.initials: D
authors.lastname: Florentino
authors.forename: Diego Zapelini
authors.initials: DZ
authors.lastname: Nascimento
authors.forename: Gislaine Tezza
authors.initials: GT
authors.lastname: Rezin
authors.forename: Daniela Dimer
authors.initials: DD
authors.lastname: Leffa
authors.forename: Jucelia Jeremias
authors.initials: JJ
authors.lastname: Fortunato
authors.forename: Felipe
authors.initials: F
authors.lastname: Dal-Pizzol
authors.forename: Tatiana
authors.initials: T
authors.lastname: Barichello
authors.forename: Joao
authors.initials: J
authors.lastname: Quevedo
authors.affiliation: Laboratorio de Fisiopatologia Clinica e Experimental, Programa de Pos-Graduacao em Ciencias da Saude, Universidade do Sul de Santa Catarina, Tubarao, SC, Brazil. fabricia.petronilho@unisul.br.
authors.forename: Fabricia
authors.initials: F
authors.lastname: Petronilho
mesh_terms: D000818:Animals; D001812:Blood-Brain Barrier / Q000473:pathology; D001921:Brain / Q000473:pathology / Q000503:physiopathology*; D002199:Capillary Permeability / Q000502:physiology; D004195:Disease Models, Animal; D009765:Obesity / Q000150:complications*; D018384:Oxidative Stress / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar; D018805:Sepsis / Q000150:complications* / Q000503:physiopathology*