The prevalence of nonalcoholic fatty liver disease (NAFLD) has increased over the decades. Lycopene (LYC), a major carotenoid present in tomato, has been previously demonstrated to possess liver-protecting and lipid-lowering bioactivities. However, the underlying mechanism of how LYC impact on the lipid metabolism in the liver is elusive. Here, we found that LYC significantly suppressed lipid accumulation in palmitate- treated HepG2 hepatocytes cell line by stimulating PPARα expression and enhanced lipolysis consequently. It has also been revealed that LYC prevented palmitate-induced mitochondrial dysfunction by improving mitochondrial complex expression and activating mitochondrial biogenesis pathway AMPK/SIRT1/PGC1α. Moreover, in line with in vitro study, LYC treatment significantly suppressed lipid accumulation and enhanced PPARα expression in western diet-feeding mice liver. LYC also enhanced the expressions of mitochondrial complexes and antioxidant related enzymes HO-1/NQO1. In conclusion, the mediating effects of LYC on mitochondrial function and PPARα signaling might play pivotal roles in its beneficial effects on NAFLD.

在过去的几十年中，非酒精性脂肪肝疾病（NAFLD）的患病率呈上升趋势。番茄红素（LYC）是番茄中的主要类胡萝卜素，先前已被证明具有保护肝脏和降低脂质的生物活性。但是，LYC如何影响肝脏脂质代谢的潜在机制尚不清楚。在这里，我们发现LYC通过刺激PPARα表达并因此增强脂解作用，显着抑制了棕榈酸酯处理的HepG2肝细胞细胞中的脂质蓄积。还已经揭示，LYC通过改善线粒体复合物表达并激活线粒体生物发生途径AMPK / SIRT1 /PGC1α来预防棕榈酸酯诱导的线粒体功能障碍。而且，符合体外一项研究表明，LYC处理可显着抑制西方饮食喂养小鼠肝脏中脂质的积累并增强PPARα的表达。LYC还增强了线粒体复合物和抗氧化剂相关酶HO-1 / NQO1的表达。总之，LYC对线粒体功能和PPARα信号传导的介导作用可能在其对NAFLD的有益作用中起关键作用。