Department of Formula Sciences, College of Korean Medicine, Dongeui University, Busan 614-052, Republic of Korea.
Department of Biomedical Engineering, Mokwon University, Daejeon 302-729, Republic of Korea.
J Ethnopharmacol. 2018 Jan 10;210:80-87. doi: 10.1016/j.jep.2017.08.032. Epub 2017 Aug 24.
Korean red ginseng (Panax ginseng C.A. Meyer, Araliaceae) has been historically used as a traditional drug for the prevention and treatment of most ageing-related diseases, such as obesity, dyslipidemia, diabetes, and cardiovascular disease. Elderly men with testosterone deficiency are strongly associated with many of the aforementioned metabolic diseases. The aim of this study was to determine the effects of ginseng on obesity and lipid metabolism in a mouse model of testosterone deficiency (castrated C57BL/6J mice).
The effects of ginseng extract (GE) on obesity and lipid metabolism in high-fat diet (HFD)-fed castrated C57BL/6J mice were examined using hematoxylin and eosin staining, serum lipid analysis, and quantitative real-time polymerase chain reaction (PCR). The effects of GE, ginsenosides, and testosterone on adipogenesis were measured using Oil Red O staining, XTT assay, and real-time PCR.
Compared with HFD mice, mice receiving HFD supplemented with GE (HFD-GE) for 8 weeks showed decreased body weight, adipose tissue mass, and adipocyte size without affecting food intake. Serum levels of triglycerides and total cholesterol were lowered in HFD-GE mice than in HFD mice. GE also markedly reduced HFD-induced hepatic lipid accumulation. Concomitantly, HFD-GE decreased mRNA expression of adipogenesis-related genes (SREBP-1C, PPARγ, FAS, SCD1, and ACC1) in visceral adipose tissues compared with HFD alone. Consistent with the in vivo data, GE and major active ginsenosides (Rb1 and Rg1) decreased lipid accumulation and mRNA expression of PPARγ, C/EBPα, and SCD1 in 3T3-L1 adipocytes compared with control. Similarly, testosterone also decreased lipid accumulation and mRNA levels of PPARγ, C/EBPα, and SCD1. These inhibitory effects were further increased by co-treatment of GE or ginsenosides with testosterone.
Our results demonstrate that ginseng can inhibit obesity and dyslipidemia in HFD-fed castrated mice, possibly by inhibiting adipogenic gene expression. In addition, our results indicate that ginseng may act like testosterone to inhibit adipogenesis, suggesting that ginseng may be able to prevent obesity, hyperlipidemia, and hepatic steatosis in men with testosterone deficiency.
韩国红参（Panax ginseng C.A. Meyer，五加科）历来被用作预防和治疗与衰老相关的大多数疾病的传统药物，如肥胖、血脂异常、糖尿病和心血管疾病。睾丸激素缺乏的老年男性与上述许多代谢性疾病密切相关。本研究旨在确定人参提取物（GE）对睾丸激素缺乏症（去势 C57BL/6J 小鼠）模型中肥胖和脂质代谢的影响。
通过苏木精和伊红染色、血清脂质分析和实时定量聚合酶链反应（PCR），研究了 GE 对高脂肪饮食（HFD）喂养去势 C57BL/6J 小鼠肥胖和脂质代谢的影响。使用油红 O 染色、XTT 测定和实时 PCR 测定了 GE、人参皂苷和睾酮对脂肪生成的影响。
与 HFD 组相比，接受 HFD 补充 8 周 GE（HFD-GE）的小鼠体重、脂肪组织质量和脂肪细胞大小降低，而不影响食物摄入量。HFD-GE 小鼠的血清甘油三酯和总胆固醇水平低于 HFD 组。GE 还显著降低了 HFD 诱导的肝脂质堆积。同时，HFD-GE 降低了内脏脂肪组织中与脂肪生成相关的基因（SREBP-1C、PPARγ、FAS、SCD1 和 ACC1）的 mRNA 表达。与体内数据一致，GE 和主要活性人参皂苷（Rb1 和 Rg1）降低了 3T3-L1 脂肪细胞中 PPARγ、C/EBPα 和 SCD1 的脂质积累和 mRNA 表达，与对照组相比。同样，睾酮也降低了 PPARγ、C/EBPα 和 SCD1 的脂质积累和 mRNA 水平。GE 或人参皂苷与睾酮联合治疗进一步增加了这些抑制作用。
我们的研究结果表明，人参可抑制 HFD 喂养去势小鼠的肥胖和血脂异常，可能通过抑制脂肪生成基因表达。此外，我们的结果表明，人参可能像睾酮一样抑制脂肪生成，这表明人参可能能够预防睾丸激素缺乏症男性的肥胖、高脂血症和肝脂肪变性。
