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通过抑制3T3-L1细胞的脂肪生成并诱导脂解、产热和自噬来抑制脂滴积累。

Inhibition of lipid droplet accumulation by by suppressing adipogenesis and inducing lipolysis, thermogenesis and autophagy in 3T3‑L1 cells.

作者信息

Choi Jeong Won, Choi Hyeok Jin, Ryu Gwang Hyeon, Lee Jae Won, Jeong Jin Boo

机构信息

Department of Forest Science, Andong National University, Andong, Gyeongsangbuk-do 36729, Republic of Korea.

出版信息

Exp Ther Med. 2023 May 19;26(1):333. doi: 10.3892/etm.2023.12032. eCollection 2023 Jul.

Abstract

It has been reported that exhibits anti-obesity effects in animal models induced by a high-fat diet. However, research on how exerts its anti-obesity effects is currently limited. Thus, the present study focused on identifying the mechanism of action associated with the anti-obesity activity of aerial part (SNAP), which significantly inhibited the accumulation of lipid droplets in differentiating 3T3-L1 cells. Intracellular lipid accumulation in 3T3-L1 cells was analyzed by Oil-Red O staining and glycerol content was analyzed using an ELISA kit. In addition, changes in protein expression within 3T3-L1 cells were analyzed using western blot analysis. It decreased the expression level of adipogenic proteins such as CCAAT/enhancer-binding protein α, Peroxisome proliferator-activated receptor γ, fatty acid binding protein 4, and adiponectin. In addition, SNAP increased the expression levels of lipolytic proteins, such as adipose triglyceride lipase and hormone-sensitive lipase, while decreasing perilipin-1. The treatment of fully differentiated 3T3-L1 cells increased the free glycerol levels. SNAP treatment resulted in increased AMP-activated protein kinase phosphorylation and the expression levels of thermogenic proteins (peroxisome proliferator-activated receptor-γ coactivator 1-α, PR domain containing 16 and uncoupling protein 1) and an autophagic protein (LC3-II). Overall, these results suggested that SNAP inhibited lipid droplet accumulation by suppressing adipogenesis and promoting lipolysis, thermogenesis and autophagy.

摘要

据报道,[具体物质]在高脂饮食诱导的动物模型中具有抗肥胖作用。然而,目前关于[具体物质]如何发挥其抗肥胖作用的研究有限。因此,本研究聚焦于确定[具体物质]地上部分(SNAP)抗肥胖活性相关的作用机制,SNAP能显著抑制分化的3T3-L1细胞中脂滴的积累。通过油红O染色分析3T3-L1细胞内的脂质积累,并使用ELISA试剂盒分析甘油含量。此外,使用蛋白质免疫印迹分析3T3-L1细胞内蛋白质表达的变化。它降低了成脂蛋白如CCAAT/增强子结合蛋白α、过氧化物酶体增殖物激活受体γ、脂肪酸结合蛋白4和脂联素的表达水平。此外,SNAP增加了脂解蛋白如脂肪甘油三酯脂肪酶和激素敏感性脂肪酶的表达水平,同时降低了围脂滴蛋白-1的表达。用SNAP处理完全分化的3T3-L1细胞可提高游离甘油水平。SNAP处理导致AMP激活的蛋白激酶磷酸化增加以及产热蛋白(过氧化物酶体增殖物激活受体γ共激活因子1-α、含PR结构域蛋白16和解偶联蛋白1)和自噬蛋白(LC3-II)的表达水平增加。总体而言这些结果表明,SNAP通过抑制脂肪生成和促进脂解、产热和自噬来抑制脂滴积累。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fe3e/10280322/086efbb26b65/etm-26-01-12032-g00.jpg

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