Ginseng seed oil ameliorates hepatic lipid accumulation in vitro and in vivo
JOURNAL OF GINSENG RESEARCH
Authors: Kim, Go Woon; Jo, Hee Kyung; Chung, Sung Hyun
Abstract
Background: Despite the large number of studies on ginseng, pharmacological activities of ginseng seed oil (GSO) have not been established. GSO is rich in unsaturated fatty acids, mostly oleic and linoleic acids. Unsaturated fatty acids are known to exert a therapeutic effect in nonalcoholic fatty liver disease (NAFLD). In this study, we investigated the protective effect and underlying mechanisms of GSO against NAFLD using in vitro and in vivo models. Methods: In vitro lipid accumulation was induced by free fatty acid mixture in HepG2 cells and by 3 wk of high fat diet (HFD)-feeding in Sprague-Dawley rats prior to hepatocyte isolation. The effects of GSO against diet-induced hepatic steatosis were further examined in C57BL/6J mice fed a HFD for 12 wk. Results: Oil Red O staining and intracellular triglyceride levels showed marked accumulation of lipid droplets in both HepG2 cells and rat hepatocytes, and these were attenuated by GSO treatment. In HFD-fed mice, GSO improved HFD-induced dyslipidemia and hepatic insulin resistance. Increased hepatic lipid contents were observed in HFD-fed mice and it was lowered in GSO (500 mg/kg)-treated mice by 26.4% which was evident in histological analysis. Pathway analysis of hepatic global gene expression indicated that GSO increased the expression of genes associated with beta-oxidation (Ppara, Ppargc1a, Sirt1, and Cpt1a) and decreased the expression of lipogenic genes (Srebf1 and Mlxipl), and these were confirmed with reverse transcription and quantitative polymerase-chain reaction. Conclusion: These findings suggest that GSO has a beneficial effect on NAFLD through the suppression of lipogenesis and stimulation of fatty acid degradation pathway. (C) 2017 The Korean Society of Ginseng, Published by Elsevier Korea LLC.
Pro-oxidant/pro-inflammatory alterations in the offsprings heart of mild diabetic rats are regulated by maternal treatments with a mitochondrial antioxidant
REPRODUCTIVE TOXICOLOGY
Authors: Higa, Romina; Roberti, Sabrina L.; Capobianco, Evangelina; Fornes, Daiana; White, Veronica; Jawerbaum, Alicia
Abstract
Maternal diabetes programs metabolic and cardiovascular diseases in the offspring. Here, we demonstrated increased pro-oxidant/pro-inflammatory markers in the heart of 2-day-old offspring of diabetic rats, previous to the induction of metabolic alterations. At a pre-pubertal stage, sex-dependent changes were evidenced in the diabetic group, as only males showed increased glycemia as well as increased concentrations of nitrated proteins, matrix metalloproteinase-9 and peroxisome proliferator activated receptor a (PPAR alpha) in the heart. Differently, the heart of male and female offspring of diabetic rats showed increased levels of connective tissue growth factor (CTGF). Maternal treatments with idebenone, a mitochondrial antioxidant, led to reductions in all the pro-oxidant and pro-inflammatory markers evaluated and in PPARa protein expression in the heart of the offspring of diabetic rats. The results of the present study highlight the gender dependence and the role of oxidative stress in the diabetes-induced intrauterine programming of heart alterations. (C) 2017 Elsevier Inc. All rights reserved.