Department of Pharmacy, Changchun University of Chinese Medicine, Changchun 130117, China.
Food Funct. 2022 Mar 21;13(6):3561-3571. doi: 10.1039/d1fo04273d.
Obesity disrupts the immune system of adipose tissue, and the activation of its macrophages constantly infiltrating adipose tissue is a crucial cause of insulin resistance induced by obesity. We previously reported for the first time that the antidiabetic effect of CK may be through the inhibition of macrophage activation and we further explored the specific mechanism . In order to clarify it, the C57BL/6J mice were fed with a high fat diet and then administered with CK orally. The related biochemical indices were detected, the inflammatory factors in serum and tissues were measured, and the related protein expression levels in insulin pathways and inflammatory signaling pathways were observed. The results showed that CK could dose-dependently reduce macrophage M1-type inflammatory factor expression in serum and adipose tissue, improve insulin resistance and glucose tolerance effectively, upregulate PPARγ expression and block TLR4/TRAF6/TAK1/NF-κB activation in obese mice. In addition, CK promoted the expression of IRS1/PI3K/AKT. Furthermore, our study showed that ginsenoside CK could improve insulin resistance by reducing inflammation through the PPARγ/NF-κB signaling pathway, which implies that ginsenoside CK may be an effective agent against obesity or early diabetes.
肥胖会扰乱脂肪组织的免疫系统，而不断浸润脂肪组织的巨噬细胞的激活是肥胖引起胰岛素抵抗的一个关键原因。我们之前首次报道称， CK 的降血糖作用可能是通过抑制巨噬细胞的激活，我们进一步探索了其具体的机制。为了阐明这一点，我们用高脂肪饮食喂养 C57BL/6J 小鼠，然后用 CK 进行口服给药。检测了相关的生化指标，测量了血清和组织中的炎症因子，并观察了胰岛素通路和炎症信号通路中相关蛋白的表达水平。结果表明， CK 能够剂量依赖性地降低肥胖小鼠血清和脂肪组织中巨噬细胞 M1 型炎症因子的表达，有效改善胰岛素抵抗和葡萄糖耐量，上调 PPARγ 的表达，并阻断 TLR4/TRAF6/TAK1/NF-κB 在肥胖小鼠中的激活。此外， CK 还促进了 IRS1/PI3K/AKT 的表达。此外，我们的研究表明，人参皂苷 CK 可以通过 PPARγ/NF-κB 信号通路减少炎症来改善胰岛素抵抗，这意味着人参皂苷 CK 可能是一种对抗肥胖或早期糖尿病的有效药物。
