Autophagy eliminates damaged cellular components. In the liver, it has been proposed that it mediates the breakdown of lipid droplets. This study aimed to compare the involvement of autophagy and the oxidative status in the effects of resveratrol and energy restriction as therapeutic tools for managing liver steatosis. In addition, potential additive or synergic effects were studied. Rats were fed a high-fat high-sucrose diet for 6 weeks and then divided into four experimental groups and fed a standard diet: a control group (C), a resveratrol-treated group (RSV, 30 mg kg⁻¹ d⁻¹), an energy restricted group (R, −15%), and an energy restricted group treated with resveratrol (RR). Liver triacylglycerols (TGs) were measured by Folch's method. TBARS, GSH, GSSG, GPx and SOD were assessed using commercial kits. The protein expression of beclin, atg5 and p62, as well as ratios of pSer555 ULK1/total ULK1, pSer757 ULK1/total ULK1 and LC3 II/I were determined by western blotting. Energy restriction increased the protein expression of beclin, atg5 and pSer757 ULK1/total ULK1 and LC3 II/I ratios, and reduced the protein expression of p62, thus indicating that it induced autophagy activation. The effects of resveratrol were similar but less marked than the hypocaloric diet. No differences were observed in oxidative stress determinants except for TBARS, which was decreased by energy restriction. In conclusion, resveratrol can reverse partially dietary-induced hepatic lipid accumulation, although less efficiently than energy restriction. The delipidating effect of energy restriction is mediated in part by the activation of autophagy; however, the involvement of this process in the effects of resveratrol is less clear.

中文翻译：

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自噬参与白藜芦醇在肝脂肪变性治疗中的有益作用。与能量限制的比较

自噬消除了受损的细胞成分。在肝脏中，已经提出它介导脂滴的分解。这项研究旨在比较自噬和氧化状态对白藜芦醇和能量限制的影响，作为治疗肝脂肪变性的治疗工具。此外，还研究了潜在的累加或协同作用。给大鼠饲喂高脂高蔗糖饮食6周，然后分为四个实验组并饲喂标准饮食：对照组（C），白藜芦醇治疗组（RSV，30 mg kg ^-1 d ^-1），能量受限组（R，-15％）和能量受限组用白藜芦醇（RR）治疗。肝三酰基甘油（TGs）通过Folch法测定。使用商业试剂盒评估了TBARS，GSH，GSSG，GPx和SOD。通过蛋白质印迹法测定beclin，atg5和p62的蛋白质表达，以及pSer555 ULK1 /总ULK1，pSer757 ULK1 /总ULK1和LC3 II / I的比率。能量限制增加了beclin，atg5和pSer757 ULK1 /总ULK1和LC3 II / I的蛋白质表达，并降低了p62的蛋白质表达，因此表明它诱导了自噬激活。白藜芦醇的作用相似，但没有低热量饮食明显。除TBARS外，在氧化应激决定簇上没有观察到差异，而TBARS由于能量限制而降低了。综上所述，白藜芦醇可部分逆转饮食引起的肝脂质蓄积，尽管效率不如能量限制。能量限制的降血脂作用部分通过自噬的激活来介导。然而，该过程是否参与白藜芦醇的作用尚不清楚。