来源于五味子的戈米辛C通过脂肪细胞中的JAK2-STAT信号通路抑制脂质积累。
S-derived gomisin C suppreses lipid accumulation by JAK2-STAT signaling in adipocyte.
作者信息
You Ye-Lim, Lee Ji-Yeon, Choi Hyeon-Son
机构信息
Department of Food Nutrition, Sangmyung University, Hongjimun 2-Gil 20, Jongno-Gu, Seoul, 03016 Republic of Korea.
出版信息
Food Sci Biotechnol. 2023 Feb 3;32(9):1225-1233. doi: 10.1007/s10068-023-01263-8. eCollection 2023 Aug.
UNLABELLED
Gomisin C is a lignan isolated from the fruit of S. The current study aimed to investigate the effect of gomisin C on lipid accumulation in adipocytes and its underlying mechanism. Gomisin C effectively inhibited lipid accumulation by downregulating adipogenic factors such as PPARγ and C/EBPα. Gomisin C-mediated suppression of lipid accumulation occurred in the early adipogenic stage; C/EBPβ was downregulated by 55%, while KLF2 was upregulated by 1.5-fold. Gomisin C significantly reduced the production of reactive oxygen species but upregulated antioxidant enzymes, including catalase, SOD1, and Gpx at the mRNA level. Gomisin C regulated NRF2-KEAP1 pathway by increasing NRF2 and decreasing KEAP1, in protein abundance. Furthermore, gomisin C suppressed the JAK2-STAT signaling pathway by decreasing phosphorylation. Taken together, gomisin C reduced early adipogenesis and ROS production by inhibiting the JAK2-STAT signaling pathway but activating the NRF2-KEAP1 signaling pathway.
SUPPLEMENTARY INFORMATION
The online version contains supplementary material available at 10.1007/s10068-023-01263-8.
未标注
五味子酯丙是从华中五味子果实中分离出的一种木脂素。本研究旨在探讨五味子酯丙对脂肪细胞脂质积累的影响及其潜在机制。五味子酯丙通过下调过氧化物酶体增殖物激活受体γ（PPARγ）和CCAAT/增强子结合蛋白α（C/EBPα）等脂肪生成因子有效抑制脂质积累。五味子酯丙介导的脂质积累抑制发生在脂肪生成早期；C/EBPβ下调55%，而 Kruppel样因子2（KLF2）上调1.5倍。五味子酯丙显著降低活性氧的产生，但在mRNA水平上调抗氧化酶，包括过氧化氢酶、超氧化物歧化酶1（SOD1）和谷胱甘肽过氧化物酶（Gpx）。五味子酯丙通过增加核因子E2相关因子2（NRF2）和减少 Kelch样ECH相关蛋白1（KEAP1）的蛋白丰度来调节NRF2-KEAP1通路。此外，五味子酯丙通过降低磷酸化来抑制Janus激酶2-信号转导和转录激活因子（JAK2-STAT）信号通路。综上所述，五味子酯丙通过抑制JAK2-STAT信号通路但激活NRF2-KEAP1信号通路来减少早期脂肪生成和活性氧的产生。
补充信息
在线版本包含可在10.1007/s10068-023-01263-8获取的补充材料。
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