Pre-fibrotic Status in the Lung of a Mouse Model of Metabolic Syndrome: Implication of Oxidative Stress and Inflammation

MIGUEL W FORNES; MARIA C DELLA VEDOVA; NIDIA N GOMEZ; SANDRA E GOMEZ MEJIBA; RAMIREZ; DC

CHICAGO

Congreso; SfRBM 2017; 2017

SFRBM

Obesity is a low-grade chronic inflammatory diseaseresulting from adipose tissue inflammation. Metabolicsyndrome (MS) is the most serious consequence of obesity.Although many organs are affected in the MS, its impact onlung biochemistry is less known. Herein we aimed atdetermining the impact of MS on redox/inflammatory statusand potential consequences in the lung using a previouslydeveloped mouse model of MS. To achieve this goal, 6week-old male C57BL / 6J mice were fed for 16 weeks witha low fat- (LFD) or a high fat-diet (HFD, chicken fat) andwater supplemented with 10% fructose (F). Thus, theexperimental design included 2 groups: LFD (control)HFD+F (MS). Compared to control, the lung parenchyma ofMS mice showed increased neutrophils content, MPOactivity, oxidative stress (NOX-2, carbonyls, TBARS andnitrotyrosine) and inflammation markers (iNOS, ICAM-1,TNF-α and IL-6). In addition and compared to LFD, the lungparenchyma of HFD+F mice had a lower total antioxidantcapacity, GSH/GSSG ratio; and activity of catalase,superoxide dismutase and glutathione peroxidase.Interestingly and compared to LFD, the lung parenchyma ofHFD+F mice had an increased pro-fibrotic status asassessed by trichromic stain and TGF-β expression. In thisstudy, we report a mouse model of MS showing lungoxidative stress/inflammation and a profibrotic status.