氢杨梅素改善高脂饮食诱导的肥胖小鼠肝脏脂肪沉积及机制（英文）

有文献报道, SIRT1-AMPK信号通路可能在DHM改善肝脏细胞甘油三酯蓄积、胰岛素抵抗等作用中发挥作用。为此,本课题拟进一步观察DHM对高脂饮食诱导的肥胖小鼠肝脏脂肪沉积的影响,并探讨其可能机制。C57BL/6J小鼠采用普通饲料和高脂饲料喂养,同时分别用或不用低剂量(125 mg/kg)或高剂量(250 mg/kg)的DHM处理16周。实验期间,每两周检测体重一次。16周后,眼眶静脉取血并处死动物,同时取肩胛下、附睾与腹股沟的脂肪并用电子秤进行称重,并记录脂肪重量。全自动生化分析仪检测:血清甘油三酯(triglyceride,TG)、血清总胆固醇(totalcholesterol,TC)、血清高密度脂蛋白(high-densitylipoprotein,HDL)、血清低密度脂蛋白(low-densitylipoprotein,LDL)。取肝脏甲醛固定、HE和油红O染色检测肝脏脂肪沉积情况;比色法检测肝脏MDA和SOD含量; Realtime PCR检测相关指标的基因表达:IL-6、IL-8、TNF-α、乙酰辅酶A羧化酶(acetyl-Co A carboxylase, ACC)、固...

Dihydromyricetin improves liver fat deposition in high-fat diet-induced obese mice

It has been reported that the histone/protein deacetylase SIRT1-AMP-activated protein kinase (SIRT1-AMPK) signaling pathway may play a role in the effects of dihydromyricetin (DHM) on improving triglyceride (TG) accumulation and insulin resistance in liver cells. Therefore, we aimed to further observe the effect of DHM on liver fat deposition in high-fat diet (HFD)-induced obese mice and explore its possible mechanism. C57BL/6J mice were fed with a normal diet (ND) and HFD and were treated with or without low-dose (125 mg/kg) or high-dose (250 mg/kg) DHM for 16 weeks, respectively. During the experiment, body weight was checked every 2 weeks. After 16 weeks, the orbital vein was bled, the animals were sacrificed, and the subscapular, epididymal, and inguinal fat were collected and weighed with an electronic scale. An automatic biochemical analyzer was used to determine the levels of serum triglyceride (TG), serum total cholesterol (TC), serum high-density lipoprotein (HDL), and serum low-density lipoprotein (LDL). The livers were stained with hematoxylin-eosin staining (H&E) and Oil Red O to detect liver fat deposition. A colorimetric method was used to detect liver MDA and SOD contents. Quantitative real-time PCR (qRT-PCR) was used to detect the gene expressions of related indicators, such as interleukin-6 (IL-6), interleukin-8 (IL-8), tumor necrosis factor-α (TNF-α), acetyl-CoA carboxyl acetyl-CoA carboxylase (ACC), sterol regulatory element-binding protein-1c (SREBP-1), fatty acid synthetase (FAS), peroxisome proliferator activation receptor alpha (peroxisome proliferator-activated receptor-alpha, PPARα), palmitoyltransferase 1 (carnitine palmitoyltransferase 1, CPT1), SIRT1, and AMPK. Western blotting analysis was used to detect the protein expression levels of SIRT1, AMPK, SIRT1-AMPK, ACC, SREBP-1, FAS, PPARα, and CPT1. Results showed that compared with the ND group, the weight and body fat of the mice in the HFD group were increased significantly. The levels of TG, TC, and LDL were increased, the level of HDL was decreased, the volume of hepatocytes was increased, the number of lipid droplets, fat deposition, MDA, IL-6, IL-8, TNF-α, SREBP-1c, FAS, ACC1, SIRT1, and AMPK protein levels were significantly increased, and the SOD activity, PPARα, CPT1, SIRT1 mRNA, AMPK mRNA, PPARα, CPT1 levels were significantly decreased. DHM could significantly reverse the changes of the above indexes in HFD mice, while DHM had no significant effect on the above indexes in ND mice. Collectively, our findings revealed that DHM improved liver fat deposition in HFD-induced obese mice, and the mechanism might be related to inhibition of oxidative stress, inflammation, lipid synthesis, and promotion of lipid decomposition.