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首页> 外文期刊>Functional Foods In Health And Disease >Molecular mechanism of intracellular lipid accumulation: Suppressive effect of PycnogenolR in liver cells
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Molecular mechanism of intracellular lipid accumulation: Suppressive effect of PycnogenolR in liver cells

机译：细胞内脂质积累的分子机制：肝细胞中Pycnognolrr的抑制作用

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Cells are physiologically ready to accumulate lipids such as triacylglycerides in the cytoplasm.?Five classes of perilipin (PLIN) family proteins are known to be involved in the process of intracellular lipid accumulation. PLIN2 is expressed ubiquitously including adipocytes, hepatocytes and macrophages. Over-expression of PLIN2 is demonstrated in the lesions of?fatty liver diseases and atherosclerosis. Suppression of PLIN2 expression prevents from developing these pathological conditions in animal models, suggesting that PLIN2 could be a therapeutic target molecule for excessive intracellular lipid accumulation which leads to various metabolic derangements. The PLIN2 gene promoter has two important cis-acting elements in close proximity:AP-1 element which mediates inflammatory signals and PPRE which mediates free fatty acid effect. In NMuLi mouse liver cells, FFA such as oleic acid requires both functional AP-1 and PPRE simultaneously to stimulate the promoter activity, indicating the presence of intimate interaction of inflammatory and metabolic signals on this gene. PycnogenolR, French maritime pine bark extracts, suppressed the oleic acid-induced PLIN2 expression and lipid accumulation in NMuLi cells. We found that PycnogenolR?did not suppress the PLIN2 promoter activity or AP-1 binding to DNA. Instead, PycnogenolR?facilitates the PLIN2 mRNA degradation, leading to suppression of lipid accumulation. This effect seems to be independent of antioxidant effect of PycnogenolR. We raise the idea that PLIN2 is a putative target molecule for prevention of pathological condition induced by?excessive lipid accumulation, and this class of natural compounds could be putative therapeutic modalities.
机译：细胞在生理学上准备好累积脂质，例如三酰基甘油酯在细胞质中。已知患有细胞内脂质积累的过程中的哌利普（PLIN）族蛋白。 Plin2普遍地表达，包括脂肪细胞，肝细胞和巨噬细胞。在脂肪肝疾病和动脉粥样硬化的病变中证明了Plin2的过表达。抑制PLIN2表达可防止在动物模型中发育这些病理条件，表明PLIN2可以是治疗靶分子，用于过量细胞内脂质积累，其导致各种代谢紊乱。 PLIN2基因启动子具有两个紧密接近的重要顺式作用元件：AP-1元素，其介导炎症信号和培养游离脂肪酸效应的PPRE。在Nmuli小鼠肝细胞中，诸如油酸的FFA需要同时刺激功能性AP-1和PPRE以刺激促进剂活性，表明存在炎症和代谢信号对该基因的紧密相互作用。碧萝芷，法国海洋松树树皮提取物，抑制了油酸诱导的荷兰细胞中的脂酸诱导的普萘2表达和脂质积累。我们发现Pycnogenolr？没有抑制PLIN2启动子活性或AP-1与DNA结合。相反，Pycnogenolr？促进PLIN2 mRNA降解，导致抑制脂质积累。这种效果似乎与Pycnognolr的抗氧化效果无关。我们提出了Plin2是用于预防由脂质积累诱导的病理病理病理病症的推定的靶分子，并且这类天然化合物可以推定治疗方式。

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