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

Authors
 Jin-Kyung Park  ;  Jae-Yong Shim  ;  A-Ra Cho  ;  Mi-Ra Cho  ;  Yong-Jae Lee 
Citation
 JOURNAL OF MEDICINAL FOOD, Vol.21(6) : 544-550, 2018 
Journal Title
JOURNAL OF MEDICINAL FOOD
ISSN
 1096-620X 
Issue Date
2018
Keywords
Korean red ginseng ; inflammation ; mitochondria ; type 2 diabetes mellitus
Abstract
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 A1c (HbA1c) 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 100 mg/kg, the fasting glucose, HbA1c, 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.
Full Text
https://www.liebertpub.com/doi/10.1089/jmf.2017.4059
DOI
10.1089/jmf.2017.4059
Appears in Collections:
6. Others (기타) > Dept. of Health Promotion (건강의학과) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Family Medicine (가정의학교실) > 1. Journal Papers
Yonsei Authors
Park, Jin-Kyung(박진경) ORCID logo https://orcid.org/0000-0002-3934-8632
Shim, Jae Yong(심재용) ORCID logo https://orcid.org/0000-0002-9561-9230
Lee, Yong Jae(이용제) ORCID logo https://orcid.org/0000-0002-6697-476X
Cho, Mi Ra(조미라)
Cho, A Ra(조아라) ORCID logo https://orcid.org/0000-0002-3645-2282
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/162507
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