Yan Dong, Wei Yuan-Yuan, Li Xiu-Mei, Sun Xiu-Chao, Wang Zhong, Aisa Haji Akber
Department of Pharmacology, Xinjiang Medical UniversityChina.
Department of Physiology, Xinjiang Medical UniversityChina.
Am J Transl Res. 2017 Jun 15;9(6):3073-3083. eCollection 2017.
High-calorie food leads to nonalcoholic fatty liver disease (NAFLD) through the dysregulation of genes involved in lipid metabolism, but the precise mechanism is still unknown. Pomegranate flowers are used to treat diabetes mellitus in traditional Uighur medicine. Here we sought to investigate the effect and mechanism of pomegranate flower polyphenols (PFP) on NAFLD Apo E mice induced by a high-fat diet (HFD) and whether PFP improves NAFLD through decreasing oxidative stress. PFP supplementation in mice significantly reduced the HFD-induced gains in body weight compared with the mice fed only with HFD. It also significantly reduced HFD-induced increases in serum lipids, including cholesterol and triglyceride. Consistent with the reduced liver weight, hepatic lipid accumulation, and the size of lipid droplets in the epididymal fat pads were also reduced by PFP supplementation. To further investigate how PFP may reduce obesity, we analyzed lipid metabolism-related genes in the liver. PFP supplementation altered expression profiles of several lipid metabolism-related genes, including ACC, AMPK, CPT-1α, FAS, LDLR, Leptin, LXR, PON1, PPAR, SirT3, and SREBP, relative to those in HFD control mice. The expression patterns of these genes observed by quantitative reverse transcriptase-polymerase chain reaction and AMPK, SirT3, ACC2, and CPT-1A expression were confirmed by immunohistochemical assays. Collectively, our results indicate that PFP prevents HFD-induced obesity in Apo E mice, and its anti-obesity effects may be related to the regulation of lipogenesis at the level of transcription.
高热量食物通过脂质代谢相关基因的失调导致非酒精性脂肪性肝病(NAFLD),但其确切机制仍不清楚。在传统维吾尔医学中,石榴花用于治疗糖尿病。在此,我们旨在研究石榴花多酚(PFP)对高脂饮食(HFD)诱导的NAFLD Apo E小鼠的作用及机制,以及PFP是否通过降低氧化应激来改善NAFLD。与仅喂食HFD的小鼠相比,给小鼠补充PFP可显著降低HFD诱导的体重增加。它还显著降低了HFD诱导的血清脂质升高,包括胆固醇和甘油三酯。与肝脏重量减轻一致,补充PFP也减少了附睾脂肪垫中的肝脏脂质积累和脂滴大小。为了进一步研究PFP如何减轻肥胖,我们分析了肝脏中与脂质代谢相关的基因。相对于HFD对照小鼠,补充PFP改变了几种与脂质代谢相关基因的表达谱,包括ACC、AMPK、CPT-1α、FAS、LDLR、瘦素、LXR、PON1、PPAR、SirT3和SREBP。通过定量逆转录聚合酶链反应观察到的这些基因的表达模式以及AMPK、SirT3、ACC2和CPT-1A的表达通过免疫组织化学分析得到证实。总体而言,我们的结果表明,PFP可预防HFD诱导的Apo E小鼠肥胖,其抗肥胖作用可能与转录水平上的脂肪生成调节有关。