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Watermelon consumption improves inflammation and antioxidant capacity in rats fed an atherogenic diet.

Abstract
Cardiovascular disease (CVD) is the leading cause of death in the United States. Watermelon, rich in antioxidants and other bioactive components, may be a viable method to improve CVD risk factors through reduced oxidative stress. The purpose of the study was to determine the effects of watermelon powder consumption on lipid profiles, antioxidant capacity, and inflammation in dextran sodium sulfate (DSS)-treated rats fed an atherogenic diet. We hypothesized that watermelon would increase antioxidant capacity and reduce blood lipids and inflammation through modulation of related gene expression. Forty male-weanling (21 days old) Sprague-Dawley rats were divided into 4 groups (10 per group, total N = 40) in a 2 diets (control or 0.33% watermelon) × 2 treatments (with or without DSS) factorial design using an atherogenic diet. Watermelon-fed groups exhibited significantly lower serum triglycerides, total cholesterol, and low-density lipoprotein cholesterol (P< .05). C-reactive protein levels were significantly lower in watermelon-fed rats than the control (P= .001). In addition, oxidative stress as measured by thiobarbituric acid reactive substances was significantly lower in watermelon groups (P= .001). Total antioxidant capacity, superoxide dismutase, and catalase activities were greater in watermelon groups (P< .05). Aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, and lactate dehydrogenase were significantly lower in DSS-treated rats when watermelon was consumed (P< .05). Fatty acid synthase, 3-hydroxy-3methyl-glutaryl-CoA reductase, sterol regulatory element-binding protein 1, sterol regulatory element-binding protein 2, and cyclooxygenase-2 gene expression was significantly downregulated in the watermelon group without DSS (P< .05). These findings indicate that watermelon improves risk factors for CVD in rats through better lipid profiles, lower inflammation, and greater antioxidant capacity by altering gene expression for lipid metabolism.
AuthorsMee Young Hong, Nicole Hartig, Katy Kaufman, Shirin Hooshmand, Arturo Figueroa, Mark Kern
JournalNutrition research (New York, N.Y.) (Nutr Res) Vol. 35 Issue 3 Pg. 251-8 (Mar 2015) ISSN: 1879-0739 [Electronic] United States
PMID25631716 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
CopyrightCopyright © 2015 Elsevier Inc. All rights reserved.
Chemical References
  • Anti-Inflammatory Agents
  • Antioxidants
  • Inflammation Mediators
  • Lipids
  • Plant Extracts
  • C-Reactive Protein
Topics
  • Animals
  • Anti-Inflammatory Agents (pharmacology, therapeutic use)
  • Antioxidants (metabolism, pharmacology, therapeutic use)
  • C-Reactive Protein (metabolism)
  • Cardiovascular Diseases (blood, etiology, prevention & control)
  • Citrullus
  • Diet, Atherogenic (adverse effects)
  • Down-Regulation
  • Fruit
  • Gene Expression (drug effects)
  • Inflammation (blood, drug therapy)
  • Inflammation Mediators (metabolism)
  • Lipids (blood)
  • Liver (drug effects, enzymology)
  • Male
  • Oxidative Stress (drug effects)
  • Phytotherapy
  • Plant Extracts (pharmacology, therapeutic use)
  • Rats, Sprague-Dawley

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