Obesity is considered a health hazard in part due to the associated multiple diseases. As rates of obesity continue to increase, a new strategy for its prevention and treatment is required. Compound-K, an active ingredient in ginseng, possesses antioxidant, anti-inflammatory, and anti-cancer properties. Although ginseng has used as various therapeutics, its potential ability to alleviate metabolic diseases by regulating adipocyte differentiation is still unknown. In this study, we found that CK treatment significantly inhibited lipid droplet and adipogenesis by downregulating the mRNA expression of C/ebpα, Ppar-γ, Fabp4, Srebp1, and adiponectin as well as protein levels of C/EBPα, PPAR-γ, and FABP4. CK also decreased the production of reactive oxygen species (ROS), while it increased endogeneous antioxidant enzymes such as catalase, glutathione peroxidase (GPx), glutathione reductase (GR), superoxide dismutase (SOD) 3 and SOD2. We observed that CK treatment suppressed the expression of cyclin-dependent kinase 1 (CDK1) and cyclin B1 during the mitotic clonal expansion (MCE) of adipocyte differentiation, and it arrested adipocytes at the G2/M stage due to the increased expression of p21 and p27. CK decreased the phosphorylation of extracellular signal-regulated kinase (ERK) and p38 and protein kinase B (AKT) in early-stage adipogenesis. In addition, the inhibition of adipogenesis by CK significantly increased the phosphorylation of AMP-activated protein kinase (AMPK) and acetyl-CoA carboxylase (ACC). Interestingly, AMPK pharmacological inhibition with Dorsomorphin limited the effect of CK on suppressing PPAR-γ expression in differentiated 3T3-L1 cells. Our results suggest that CK exerts anti-adipogenic effects in 3T3-L1 cells through the activation of AMPK and inhibition of ERK/p38 and AKT signaling pathways.

中文翻译：

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人参皂苷 CK 通过 AMPK、MAPK 和 AKT 信号通路抑制脂肪生成的早期阶段

肥胖被认为是一种健康危害，部分原因是相关的多种疾病。随着肥胖率的不断增加，需要一种新的预防和治疗策略。Compound-K 是人参中的一种活性成分，具有抗氧化、抗炎和抗癌的特性。尽管人参已被用作各种治疗剂，但其通过调节脂肪细胞分化来缓解代谢疾病的潜在能力仍然未知。在本研究中，我们发现 CK 处理通过下调 C/ebpα、Ppar-γ、Fabp4、Srebp1 和脂联素的 mRNA 表达以及 C/EBPα、PPAR-γ 和FABP4。CK 还减少了活性氧 (ROS) 的产生，同时增加了内源性抗氧化酶，如过氧化氢酶、谷胱甘肽过氧化物酶 (GPx)、谷胱甘肽还原酶 (GR)、超氧化物歧化酶 (SOD) 3 和 SOD2。我们观察到 CK 处理在脂肪细胞分化的有丝分裂克隆扩增 (MCE) 期间抑制细胞周期蛋白依赖性激酶 1 (CDK1) 和细胞周期蛋白 B1 的表达，并且由于 p21 和第 27 页。CK 降低了早期脂肪生成过程中细胞外信号调节激酶 (ERK) 和 p38 和蛋白激酶 B (AKT) 的磷酸化。此外，CK 对脂肪生成的抑制显着增加了 AMP 活化蛋白激酶 (AMPK) 和乙酰辅酶 A 羧化酶 (ACC) 的磷酸化。有趣的是，用 Dorsomorphin 对 AMPK 的药理抑制作用限制了 CK 抑制分化的 3T3-L1 细胞中 PPAR-γ 表达的作用。