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提取物(CQR-300)通过下调3T3-L1细胞中的脂肪生成和脂质生成来抑制脂质积累。

extract (CQR-300) inhibits lipid accumulation by downregulating adipogenesis and lipogenesis in 3T3-L1 cells.

作者信息

Lee Hae Jin, Le Bao, Lee Dong-Ryung, Choi Bong-Keun, Yang Seung Hwan

机构信息

Department of Biotechnology, Chonnam National University, Yeosu 59626, Republic of Korea.

Nutrapharm Tech, Jungwon-gu, Seongnam, Gyeonggi 13201, Republic of Korea.

出版信息

Toxicol Rep. 2018 Mar 30;5:608-614. doi: 10.1016/j.toxrep.2018.02.008. eCollection 2018.

DOI:10.1016/j.toxrep.2018.02.008
PMID:29854631
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5977379/
Abstract

The objective of this study was to evaluate the anti-obesity activity and the action mechanism of extracts (CQR-300) in 3T3-L1 adipocytes. was extracted with hot water, resulting in CQR-300. The anti-obesity activity of CQR-300 in 3T3-L1 adipocytes was examined by Oil-red O staining. Possible mechanisms of CQR-300 in 3T3-L1 adipocytes were determined by real-time PCR and western blot. Treatment with CQR-300 inhibited lipid accumulation without showing cytotoxicity to 3T3-L1 adipocytes. Furthermore, CQR-300 decreased adipogenesis/lipogenesis-related mRNA expression levels of fatty acid binding protein (aP2), fatty acid synthase (FAS), lipoprotein lipase (LPL), stearoyl-CoA desaturase-1 (SCD-1), and acetyl-CoA carboxylase (ACC). CQR-300 also down-regulated expression levels of adipogenesis/lipogenesis-associated proteins, including peroxisome proliferator-activated receptor γ (PPARγ), CCAAT/enhancer-binding protein α (C/EBPα), sterol regulatory element binding protein-1c (SREBP-1c), and FAS. It's also up-regulated the expression level of phosphorylated-AMPK (p-AMPK). Collectively, these results suggested that CQR-300 might have an anti-obesity effect by its ability to decrease expression levels of adipogenesis/lipogenesis-related genes and proteins.

摘要

本研究的目的是评估提取物(CQR - 300)在3T3 - L1脂肪细胞中的抗肥胖活性及其作用机制。用热水提取得到CQR - 300。通过油红O染色检测CQR - 300在3T3 - L1脂肪细胞中的抗肥胖活性。通过实时PCR和蛋白质印迹法确定CQR - 300在3T3 - L1脂肪细胞中的可能作用机制。用CQR - 300处理可抑制脂质积累,且对3T3 - L1脂肪细胞无细胞毒性。此外,CQR - 300降低了脂肪酸结合蛋白(aP2)、脂肪酸合酶(FAS)、脂蛋白脂肪酶(LPL)、硬脂酰辅酶A去饱和酶-1(SCD - 1)和乙酰辅酶A羧化酶(ACC)等脂肪生成/脂质生成相关mRNA的表达水平。CQR - 300还下调了脂肪生成/脂质生成相关蛋白的表达水平,包括过氧化物酶体增殖物激活受体γ(PPARγ)、CCAAT/增强子结合蛋白α(C/EBPα)、固醇调节元件结合蛋白-1c(SREBP - 1c)和FAS。它还上调了磷酸化-AMPK(p - AMPK)的表达水平。总体而言,这些结果表明CQR - 300可能通过降低脂肪生成/脂质生成相关基因和蛋白的表达水平而具有抗肥胖作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d0a2/5977379/041da4c86a90/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d0a2/5977379/04087e2c0eb1/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d0a2/5977379/b4e7b0a53fa1/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d0a2/5977379/09b3261fa348/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d0a2/5977379/ce169443fcff/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d0a2/5977379/041da4c86a90/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d0a2/5977379/04087e2c0eb1/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d0a2/5977379/b4e7b0a53fa1/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d0a2/5977379/09b3261fa348/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d0a2/5977379/ce169443fcff/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d0a2/5977379/041da4c86a90/gr5.jpg

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