| Literature DB >> 27645696 |
Fabricia Petronilho1, Amanda Della Giustina2, Diego Zapelini Nascimento2, Graciela Freitas Zarbato2, Andriele Aparecida Vieira2, Drielly Florentino2, Lucinéia Gainski Danielski2, Mariana Pereira Goldim2, Gislaine Tezza Rezin2, Tatiana Barichello3,4.
Abstract
Sepsis progression is linked to the imbalance between reactive oxygen species and antioxidant enzymes. Sepsis affects multiple organs, but when associated with a chronic inflammatory disease, such as obesity, it may be exacerbated. We hypothesized that obesity could aggravate the oxidative damage to peripheral organs of rats submitted to an animal model of sepsis. Male Wistar rats aged 8 weeks received hypercaloric nutrition for 2 months to induce obesity. Sepsis was induced by cecal ligation and puncture (CLP) procedure, and sham-operated rats were considered as control group. The experimental groups were divided into sham + eutrophic, sham + obese, CLP + eutrophic, and CLP + obese. Twelve and 24 h after surgery, oxidative damage to lipids and proteins and superoxide dismutase (SOD) and catalase (CAT) activities were evaluated in the liver, lung, kidney, and heart. The data indicate that obese rats subjected to sepsis present oxidative stress mainly in the lung and liver. This alteration reflected an oxidative damage to lipids and proteins and an imbalance of SOD and CAT levels, especially 24 h after sepsis. It follows that obesity due to its pro-inflammatory phenotype can aggravate sepsis-induced damage in peripheral organs.Entities:
Keywords: inflammation; obesity; organs; oxidative stress; sepsis
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Year: 2016 PMID: 27645696 DOI: 10.1007/s10753-016-0444-x
Source DB: PubMed Journal: Inflammation ISSN: 0360-3997 Impact factor: 4.092