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An Herbal Formula LI85008F Inhibits Lipogenesis in 3T3-L1 Adipocytes

机译:草药配方LI85008F抑制3T3-L1脂肪细胞中的脂肪生成

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The present study demonstrates a novel herbal formulation LI85008F inhibiting adipocyte differentiation and potentiates lipolysis in 3T3-L1 mouse adipocytes. LI85008F is formulated by combining extracts of three Indian herbs Moringa oleifera, Murraya koenigii and Curcuma longa. Oil red O staining of 3T3-L1 adipocytes reveals that LI85008F is a synergistic formulation that inhibits adipocyte differentiation in a dose dependent manner and concurrently down regulates the key adipogenic transcription factors Peroxisome Proliferator-Activated Receptor gamma (PPAR) and CCAAT/enhancer binding protein α (C/EBP). LI85008F confers significant reductions in intracellular triglyceride content in a dose dependent manner. Evidence suggests that LI85008F antagonizes PPAR through Ser112 phosphorylation via MAPK/ERK activation. Immunoblot analyses reveal that LI85008F treatment also down regulates the protein expressions of key PPAR responsive gene products such as Adipocyte differentiation related protein (ADRP), CD36, Adipocyte specific binding protein 2 (aP2) and perilipin. In differentiated adipocytes culture, LI85008F treatment results in significantly (p = 0.0169) increased lipolysis as measured by the release of glycerol. LI85008F does not exhibit cytotoxic effect on adipocytes. Taken together, the results suggest that LI85008F inhibits lipogenesis in adipocytes and concurrently antagonizes PPAR? and other lipogenic factors and in addition, potentiates triglyceride mobilization from the fat cells or enhances lipolysis.
机译:本研究证明了一种新颖的草药制剂LI85008F抑制脂肪细胞分化并增强3T3-L1小鼠脂肪细胞中的脂解作用。 LI85008F是将三种印度草药辣木,辣木和姜黄的提取物组合而成。 3T3-L1脂肪细胞的油红O染色显示LI85008F是一种协同制剂,以剂量依赖性方式抑制脂肪细胞分化并同时下调关键的脂肪形成转录因子过氧化物酶体增殖物激活受体γ(PPAR)和CCAAT /增强子结合蛋白α (C / EBP)。 LI85008F以剂量依赖性方式使细胞内甘油三酸酯含量显着降低。有证据表明,LI85008F通过MAPK / ERK激活通过Ser112磷酸化来拮抗PPAR。免疫印迹分析表明,LI85008F处理还下调了关键PPAR反应基因产物的蛋白质表达,例如脂肪细胞分化相关蛋白(ADRP),CD36,脂肪细胞特异性结合蛋白2(aP2)和周脂蛋白。在分化的脂肪细胞培养中,LI85008F处理可导致甘油分解显着(p = 0.0169)的脂解增加。 LI85008F对脂肪细胞没有细胞毒性作用。两者合计,结果表明LI85008F抑制脂肪细胞中的脂肪生成并同时拮抗PPAR?和其他脂肪形成因子,此外,还可以增强脂肪细胞中的甘油三酸酯动员或增强脂解作用。

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