451. Wild ginseng cambial meristematic cells ameliorate hepatic steatosis and mitochondrial dysfunction in high-fat diet-fed mice.
- Author
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Lee SB, Cho HI, Jin YW, Lee EK, Ahn JY, and Lee SM
- Subjects
- Animals, Basic Helix-Loop-Helix Leucine Zipper Transcription Factors, Body Weight drug effects, Carnitine O-Palmitoyltransferase metabolism, Cholesterol blood, Cholesterol metabolism, DNA-Binding Proteins metabolism, Fatty Liver blood, Fatty Liver metabolism, Glutathione metabolism, High Mobility Group Proteins metabolism, Lipid Metabolism drug effects, Lipid Peroxidation drug effects, Male, Mice, Mice, Inbred C57BL, Mitochondrial Diseases blood, Mitochondrial Diseases metabolism, Non-alcoholic Fatty Liver Disease blood, Non-alcoholic Fatty Liver Disease drug therapy, Non-alcoholic Fatty Liver Disease metabolism, Nuclear Proteins metabolism, Nuclear Respiratory Factor 1 metabolism, Organelle Biogenesis, PPAR alpha metabolism, RNA-Binding Proteins metabolism, Sterol Regulatory Element Binding Protein 1 metabolism, Transaminases metabolism, Transcription Factors metabolism, Triglycerides blood, Diet, High-Fat adverse effects, Fatty Liver drug therapy, Mitochondrial Diseases drug therapy, Panax chemistry
- Abstract
Objectives: The aim of this study was to determine the protective mechanisms of wild ginseng cambial meristematic cells (CMCs) on non-alcoholic fatty liver disease in high-fat diet (HFD)-fed mice., Methods: Male C57BL/6 mice received either normal-fat diet or HFD for 10 weeks along with wild ginseng CMCs (75, 150 and 300 mg/kg) or vehicle (0.5% carboxyl methyl cellulose) by oral administration once a day. Triglyceride and total cholesterol contents were measured in liver and serum samples. Parameters for hepatic lipid metabolism and mitochondria biogenesis were assessed., Key Findings: Treatment with wild ginseng CMCs markedly attenuated body weight, serum and hepatic lipid contents, and serum aminotransferase activity. While wild ginseng CMCs attenuated the increases in sterol regulatory element-binding transcription factor 1 (SREBP-1) and carbohydrate-responsive element-binding protein (ChREBP) expression, it enhanced the increases in carnitine palmitoyltransferase 1A (CPT1A) and peroxisome proliferator-activated receptor alpha (PPAR-α) expression. HFD decreased glutamate dehydrogenase activity and glutathione content, and increased lipid peroxidation, which were all attenuated by wild ginseng CMCs. Furthermore, wild ginseng CMCs enhanced mitochondrial biogenesis-related factors, including peroxisome proliferator-activated receptor-γ co activator 1α (PGC1α), nuclear respiratory factor 1 (NRF1) and mitochondrial transcription factor A (TFAM)., Conclusions: Wild ginseng CMCs protect against HFD-induced liver injury, which prevents lipid accumulation and mitochondrial oxidative stress, and enhances mitochondrial biogenesis., (© 2015 Royal Pharmaceutical Society.)
- Published
- 2016
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