Wild ginseng cambial meristematic cells ameliorate hepatic steatosis and mitochondrial dysfunction in high-fat diet-fed mice

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.

Keywords: de-novo lipogenesis; mitochondrial biogenesis; non-alcoholic fatty liver disease; wild ginseng cambial meristematic cells; β-oxidation.