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首页> 外文期刊>Journal of Agricultural and Food Chemistry >Pterostilbene Improves Hepatic Lipid Accumulation via the MiR-34a/Sirt1/SREBP-1 Pathway in Fructose-Fed Rats
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Pterostilbene Improves Hepatic Lipid Accumulation via the MiR-34a/Sirt1/SREBP-1 Pathway in Fructose-Fed Rats

机译：活体通过MiR-34a / sirt1 / srebp-1途径在果糖喂养大鼠中改善肝脂肪积累

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High fructose intake promotes hepatic lipid accumulation. Pterostilbene, a natural analogue of resveratrol found in diet berries, exhibits a hepatoprotective property. Here, we studied the protection by pterostilbene against fructose-induced hepatic lipid accumulation and explored its possible mechanism. We observed a high expression of microRNA-34a (miR-34a, P < 0.05) and a low expression of its target, sirtuin1 (Sirt1, mRNA: P < 0.01; protein: P < 0.001), with the overactivation of downstream sterol regulatory element-binding protein-1 (SREBP-1) lipogenic pathway (nuclear SREBP-1 protein: P < 0.05; FAS and SCD1 mRNA: P < 0.01), in rat livers, as well as BRL-3A and HepG2 cells, stimulated by fructose. More interestingly, pterostilbene recovered the fructose-disturbed miR-34a expression (0.3-0.5-fold vs fructose control, P < 0.05), Sirt1 protein level (1.2- to 1.5-fold vs fructose control, P < 0.05), and SREBP-1 lipogenic pathway, resulting in significant amelioration of hepatocyte lipid accumulation in animal [hepatic triglyceride and total cholesterol (TG&TC) mg/gwet tissue: 4.90 +/- 0.19, 5.23 +/- 0.16, 5.20 +/- 0.29 vs fructose control 9.73 +/- 1.06, P < 0.001; 3.18 +/- 0.30, 3.31 +/- 0.39, 3.37 +/- 0.47 vs 5.67 +/- 0.28, P < 0.001] and cell models (BRL-3A TG&TC mmol/g-protein: 0.123 +/- 0.011 vs 0.177 +/- 0.004, P < 0.001; 0.169 +/- 0.011 vs 0.202 +/- 0.008, P < 0.05; HepG2: 0.257 +/- 0.005 vs 0.303 +/- 0.016, P < 0.05; 0.143 +/- 0.004 vs 0.201 +/- 0.008, P < 0.001). These results provide the experimental evidence supporting the anti-lipogenic effect of pterostilbene against fructose-induced hepatic lipid accumulation via modulating the miR-34a/Sirtl/SREBP-1 pathway.
机译：高果糖摄入促进肝脂积累。 Pterostilbene是白藜芦醇的天然类似物，在饮食浆果中发现，表现出肝脏保护性。在这里，我们研究了运动蛋白对果糖诱导的肝脂肪积累的保护，并探讨了可能的机制。我们观察到MicroRNA-34a的高表达（miR-34a，p <0.05）和其目标的低表达，sirtuin1（sirt1，mRNA：p <0.01;蛋白质：p <0.001），过度激活下游甾醇调节元素结合蛋白-1（srebp-1）脂肪原途径（核Srebp-1蛋白：p <0.05; fas和scd1 mRNA：p <0.01），在大鼠肝脏以及brl-3a和hepg2细胞上刺激果糖。更有趣的是，活体替补果糖干扰的miR-34a表达（0.3-0.5倍对果糖对照，P <0.05），SIRT1蛋白水平（1.2-至1.5倍对果糖对照，P <0.05）和Srebp- 1脂质途径，导致动物中肝细胞脂质积累的显着改善[肝甘油三酯和总胆固醇（TG＆Tc）mg / gwet组织：4.90 +/- 0.19,5.23 +/- 0.16,5.20 +/- 0.29 Vs果糖控制9.73 + / - 1.06，P <0.001; 3.18 +/- 0.39,3.31 +/- 0.39,3.37 +/- 0.47 Vs 5.67 +/- 0.28，P <0.001]和细胞型号（BRL-3A TG＆TC MMOL / G蛋白：0.123 +/- 0.011 VS 0.177 + / - 0.004，P <0.001; 0.169 +/- 0.011 Vs 0.202 +/- 0.008，P <0.05; Hepg2：0.257 +/- 0.005 Vs 0.303 +/- 0.016，P <0.05; 0.143 +/- 0.004 VS 0.201 + / - 0.008，p <0.001）。这些结果提供了通过调节miR-34a / sirtl / srebp-1途径调节miR-34a / sirtl / srebp-1途径，提供支持运动诱导肝脂肪积累的抗脂肪原效应的实验证据。

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