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碧萝芷®通过调节与抗氧化酶反应相关的活性氧 (ROS) 产生来抑制 3T3-L1 脂肪细胞中的脂质积累。

Pycnogenol® inhibits lipid accumulation in 3T3-L1 adipocytes with the modulation of reactive oxygen species (ROS) production associated with antioxidant enzyme responses.

机构信息

Department of Food Science and Biotechnology, Kangwon National University, Chuncheon 200-701, South Korea.

出版信息

Phytother Res. 2012 Mar;26(3):403-11. doi: 10.1002/ptr.3568. Epub 2011 Jul 27.

Abstract

Pycnogenol® is a group of flavonoids with antioxidant effects. Adipogenesis is the process of adipocyte differentiation. It causes the increase of lipids as well as ROS (reactive oxygen species). Lipid accumulation and ROS production were determined in 3 T3-L1 adipocyte, and the effect of Pycnogenol® was evaluated. Lipid accumulation was elevated in adipocyte treated with hydrogen peroxide, one of the ROS. Pycnogenol® showed an inhibitory effect on the lipid accumulation and ROS production during the adipogenesis. We also investigated the molecular events associated with ROS production and lipid accumulation. Our results showed that Pycnogenol® inhibited the mRNA expression of pro-oxidant enzymes, such as NOX4 (NADPH (nicotinamide adenine dinucleotide phosphate hydrogen) oxidase 4), and the NADPH-producing G6PDH (glucose-6-phosphate dehydrogenase) enzyme. In addition, Pycnogenol® suppressed the mRNA abundance of adipogenic transcription factors, PPAR-γ (peroxisome proliferator-activated receptor γ) and C/EBP-α (CCAAT/enhancer binding protein α), and their target gene, aP2 (adipocyte protein 2) responsible for fatty acid transportation. On the other hand, Pycnogenol® increased the abundance of antioxidant proteins such as Cu/Zn-SOD (copper-zinc superoxide dismutase), Mn-SOD (manganese superoxide dismutase), GPx (glutathione peroxidase) and GR (glutathione reductase). Our results suggest that Pycnogenol® inhibits lipid accumulation and ROS production by regulating adipogenic gene expression and pro-/antioxidant enzyme responses in adipocytes.

摘要

碧萝芷®是具有抗氧化作用的一组类黄酮。脂肪生成是脂肪细胞分化的过程。它会导致脂质以及 ROS(活性氧)的增加。在 3T3-L1 脂肪细胞中测定了脂质积累和 ROS 的产生,并评估了碧萝芷®的作用。用 ROS 之一的过氧化氢处理脂肪细胞会导致脂质积累增加。碧萝芷®在脂肪生成过程中显示出抑制脂质积累和 ROS 产生的作用。我们还研究了与 ROS 产生和脂质积累相关的分子事件。我们的结果表明,碧萝芷®抑制了促氧化剂酶(如 NADPH(烟酰胺腺嘌呤二核苷酸磷酸氢)氧化酶 4(NOX4)和 NADPH 产生酶葡萄糖-6-磷酸脱氢酶(G6PDH)的 mRNA 表达。此外,碧萝芷®抑制了脂肪生成转录因子 PPAR-γ(过氧化物酶体增殖物激活受体 γ)和 C/EBP-α(CCAAT/增强子结合蛋白 α)及其靶基因 aP2(脂肪细胞蛋白 2)的 mRNA 丰度,该基因负责脂肪酸转运。另一方面,碧萝芷®增加了抗氧化蛋白的丰度,如 Cu/Zn-SOD(铜锌超氧化物歧化酶)、Mn-SOD(锰超氧化物歧化酶)、GPx(谷胱甘肽过氧化物酶)和 GR(谷胱甘肽还原酶)。我们的结果表明,碧萝芷®通过调节脂肪生成基因表达和脂肪细胞中促氧化剂/抗氧化酶的反应来抑制脂质积累和 ROS 的产生。

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