Rosa Mosqueta Oil Prevents Oxidative Stress and Inflammation through the Upregulation of PPAR-α and NRF2 in C57BL/6J Mice Fed a High-Fat Diet

• Published in: The Journal of nutrition Vol. 147; no. 4; pp. 579 - 588
• Main Authors: González-Mañán, Daniel, D'Espessailles, Amanda, Dossi, Camila G, San Martín, Marcela, Mancilla, Rodrigo A, Tapia, Gladys S
• Format: Journal Article
• Language: English
• Published: United States 01.04.2017
• Subjects: Animals; Blood Glucose; Dietary Fats - administration & dosage; Dietary Fats - adverse effects; Heme Oxygenase-1 - genetics; Heme Oxygenase-1 - metabolism; Inflammation - drug therapy; Insulin - blood; Liver - drug effects; Liver - metabolism; Male; Mice; Mice, Inbred C57BL; NF-E2-Related Factor 2 - genetics; NF-E2-Related Factor 2 - metabolism; Oxidative Stress - drug effects; Plant Oils - chemistry; Plant Oils - pharmacology; PPAR alpha - genetics; PPAR alpha - metabolism; Rosa - chemistry; Up-Regulation; NRF2; PPAR-α; inflammation; oxidative stress; rosa mosqueta
• ISSN: 0022-3166; 1541-6100; 1541-6100
• DOI: 10.3945/jn.116.243261

Rosa mosqueta (RM) oil is characterized by high concentrations of antioxidants and α-linolenic acid (ALA; 18:3n-3). We have previously demonstrated in male C57BL/6J mice that RM decreases hepatic steatosis, a condition strongly associated with oxidative stress and inflammation. We studied the molecular mechanisms that underlie the role of RM in preventing high-fat diet (HFD)-induced oxidative stress and inflammation. Male C57BL/6J mice aged 28 d and weighing 12-14 g were divided into the following groups and fed for 12 wk: control diet (CD; 10% fat, 20% protein, and 70% carbohydrates); CD + RM (1.94 mg ALA ⋅ g body weight ⋅ d administered by oral gavage); HFD (60% fat, 20% protein, and 20% carbohydrates); and HFD + RM. General parameters (body weight, visceral fat, and histology); glucose metabolism [homeostasis model assessment and blood glucose area under the curve (AUC)]; oxidative stress [hepatic nuclear factor (erythroid-derived 2)-like-2 (NRF2) and heme oxygenase 1 (HO-1) concentrations]; and inflammation [hepatic peroxisome proliferator-activated receptor α (PPAR-α) and acyl-coenzyme A oxidase 1 (ACOX1) concentrations, blood tumor necrosis factor α (TNF-α) and interleukin 1β (IL-1β) concentrations, and and mRNA expression in liver and visceral adipose tissue] were evaluated. In the HFD + RM mice, the final body weight (24.8 ± 1.1 g) was 19% lower than in the HFD mice (30.6 ± 2.8 g) ( < 0.05). Visceral fat was 34% lower in the HFD + RM mice than in the HFD mice ( < 0.05). The blood glucose AUC was 29% lower and and expression levels were 47% and 59% lower, respectively, in the HFD + RM mice than in the HFD mice ( < 0.05). HFD + RM mice had 40% less hepatic steatosis ( < 0.05) and lower upregulation of PPAR-α (33%), ACOX1 (50%), NRF2 (39%), and HO-1 (68%) protein concentrations than did the HFD mice ( < 0.05). Our findings suggest that RM supplementation prevents the obese phenotype observed in HFD-fed mice by downregulating inflammatory cytokine expression and secretion and stimulating hepatic antioxidant and fatty acid oxidation markers.