A High-Fat Diet Increases Oxidative Renal Injury and Protein Glycation in D-Galactose-Induced Aging Rats and Its Prevention by Korea Red Ginseng

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  • PARK Sok
    Division of Sports Industry & Science, Mokwon University
  • KIM Chan-Sik
    Korean Medicine Based Herbal Drug Development Group, Herbal Medicine Research Division, Korea Institute of Oriental Medicine Department of Physiology, Ajou University School of Medicine
  • MIN Jinah
    Department of Exercise Nutrition, Teachers College, Kyungpook National University
  • LEE Soo Hwan
    Department of Physiology, Ajou University School of Medicine
  • JUNG Yi-Sook
    Department of Pathophysiology, College of Pharmacy, Ajou University Research Institute of Pharmaceutical Sciences and Technology, Ajou University

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  • A High-Fat Diet Increases Oxidative Renal Injury and Protein Glycation in <small>D</small>-Galactose-Induced Aging Rats and Its Prevention by Korea Red Ginseng

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Declining renal function is commonly observed with age. Obesity induced by a high-fat diet (HFD) may reduce renal function. Korean red ginseng (KRG) has been reported to ameliorate oxidative tissue injury and have an anti-aging effect. This study was designed to investigate whether HFD would accelerate the D-galactose-induced aging process in the rat kidney and to examine the preventive effect of KRG on HFD and D-galactose-induced aging-related renal injury. When rats with D-galactose-induced aging were fed an HFD for 9 wk, enhanced oxidative DNA damage, renal cell apoptosis, protein glycation, and extracellular high mobility group box 1 protein (HMGB1), a signal of tissue damage, were observed in renal glomerular cells and tubular epithelial cells. However, treatment of rats with HFD- plus D-galactose-induced aging with KRG restored all of these renal changes. Our data suggested that a long-term HFD may enhance D-galactose-induced oxidative renal injury in rats and that this age-related renal injury could be suppressed by KRG through the repression of oxidative injury.

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