4.4 Article

Korean Red Ginseng Protects Against Mitochondrial Damage and Intracellular Inflammation in an Animal Model of Type 2 Diabetes Mellitus

Journal

JOURNAL OF MEDICINAL FOOD
Volume 21, Issue 6, Pages 544-550

Publisher

MARY ANN LIEBERT, INC
DOI: 10.1089/jmf.2017.4059

Keywords

inflammation; Korean red ginseng; mitochondria; type 2 diabetes mellitus

Funding

  1. Yonsei University College of Medicine [6-2009-0097]

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Korean red ginseng (KRG), a heat-processed Korean ginseng (Panax ginseng C.A. Meyer), has been used as a traditional medicine for its beneficial effects on hyperglycemia. This study aimed to investigate whether the antidiabetic action of KRG in an animal model of type 2 diabetes mellitus (DM) is partly mediated by prevention of mitochondrial dysfunction and intracellular inflammation. Four-week-old C57BL/KsJ db/db mice (a genetic animal model of obese type 2 DM) and C57BL/KsJ db/+ mice were divided into three groups: db/+ mice (normoglycemic control group, n=8), db/db mice (untreated DM group, n=8), and db/db mice with KRG administration (KRG-treated DM group, n=8). After 12 weeks, metabolic parameters of fasting blood glucose concentrations, hemoglobin A(1c) (HbA(1c)) level, insulin level, lipid profile, and leukocyte count were determined using high-performance liquid chromatography. Mitochondrial DNA (mtDNA) copy number and inflammatory marker (interleukin-6, cyclooxygenase-2, and C-reactive protein) expression levels were measured in skeletal muscle tissue using quantitative real-time PCR analysis. After 12 weeks of KRG treatment at 100mg/kg, the fasting glucose, HbA(1c), insulin, and low-density lipoprotein cholesterol concentrations were lower, whereas mtDNA copy numbers were higher in the KRG-treated DM group than in the untreated DM group. Compared with the untreated DM group, the messenger RNA expression levels of mitochondrial biogenesis-related transcription factors and inflammatory markers were lower in the KRG-treated DM group. In conclusion, KRG had a beneficial effect on the metabolic profile by preserving mitochondrial function and protecting against intracellular inflammation.

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