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传统韩国草药配方三芪通过调节 3T3-L1 细胞中 ERK1/2 的磷酸化来抑制脂肪生成。

Traditional Korean Herbal Formula Samsoeum Attenuates Adipogenesis by Regulating the Phosphorylation of ERK1/2 in 3T3-L1 Cells.

机构信息

KM Convergence Research Division, Korea Institute of Oriental Medicine, Daejeon 305-811, Republic of Korea ; Korean Medicine Life Science, University of Science & Technology, Daejeon 305-350, Republic of Korea.

K-Herb Research Center, Korea Institute of Oriental Medicine, Daejeon 305-811, Republic of Korea.

出版信息

Evid Based Complement Alternat Med. 2015;2015:893934. doi: 10.1155/2015/893934. Epub 2015 Sep 21.

Abstract

Adipogenesis is the cell differentiation process from preadipocytes into adipocytes and the critical action in the development of obesity. In the present study, we conducted in vitro analyses to investigate the inhibitory effects of Samsoeum (SSE), a traditional herbal decoction. SSE had no significant cytotoxic effect against either the undifferentiated or differentiated 3T3-L1 cells. Oil Red O staining results showed that SSE significantly inhibited fat accumulation in adipocytes. SSE treatment consistently reduced the intracellular triglyceride content in the cells. SSE significantly inactivated glycerol-3-phosphate dehydrogenase (GPDH), a major link between carbohydrate and lipid metabolisms in 3T3-L1 adipocytes, and markedly inhibited the production of leptin, an important adipokine, in differentiated cells. SSE markedly suppressed the mRNA expression of the adipogenesis-related genes peroxisome proliferator-activated receptor-gamma (PPAR-γ), CCAAT/enhancer binding protein-alpha (C/EBP-α), fatty acid synthase (FAS), lipoprotein lipase (LPL), and fatty acid binding protein 4 (FABP4). Importantly, SSE increased the phosphorylation of ERK1/2, but not p38 MAPK and JNK, in adipose cells. Overall, our results indicate that SSE exerts antiadipogenic activity and modulates expressions of adipogenesis-related genes and ERK1/2 activation in adipocytes.

摘要

脂肪生成是前体脂肪细胞分化为脂肪细胞的过程,也是肥胖发生的关键。在本研究中,我们进行了体外分析,以研究一种传统草药方剂 Samsoeum(SSE)的抑制作用。SSE 对未分化或分化的 3T3-L1 细胞均无明显的细胞毒性作用。油红 O 染色结果表明,SSE 可显著抑制脂肪细胞中的脂肪堆积。SSE 处理一致降低了细胞内的甘油三酯含量。SSE 显著失活了甘油-3-磷酸脱氢酶(GPDH),这是 3T3-L1 脂肪细胞中碳水化合物和脂质代谢的主要连接酶,并且明显抑制了分化细胞中瘦素的产生,瘦素是一种重要的脂肪细胞因子。SSE 显著抑制了与脂肪生成相关的基因过氧化物酶体增殖物激活受体-γ(PPAR-γ)、CCAAT/增强子结合蛋白-α(C/EBP-α)、脂肪酸合酶(FAS)、脂蛋白脂肪酶(LPL)和脂肪酸结合蛋白 4(FABP4)的 mRNA 表达。重要的是,SSE 增加了脂肪细胞中 ERK1/2 的磷酸化,但不增加 p38 MAPK 和 JNK 的磷酸化。总的来说,我们的结果表明,SSE 具有抗脂肪生成活性,并调节脂肪细胞中与脂肪生成相关的基因表达和 ERK1/2 的激活。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e24/4592915/a948f5006085/ECAM2015-893934.001.jpg

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