Liu Hui-Kang, Hung Tzu-Min, Huang Hsiu-Chen, Lee I-Jung, Chang Chia-Chuan, Cheng Jing-Jy, Lin Lie-Chwen, Huang Cheng
National Research Institute of Chinese Medicine, Taipei 11221, Taiwan ; Ph.D. Program for the Clinical Drug Discovery from Botanical Herbs, Taipei Medical University, Taipei 11031, Taiwan.
Department of Medical Research, E-DA Hospital, Kaohsiung 82445, Taiwan.
Evid Based Complement Alternat Med. 2015;2015:651734. doi: 10.1155/2015/651734. Epub 2015 Oct 5.
Obesity and associated conditions, such as type 2 diabetes mellitus (T2DM) and nonalcoholic fatty liver disease (NAFLD), are currently a worldwide health problem. In Asian traditional medicine, Bai-Hu-Jia-Ren-Shen-Tang (BHJRST) is widely used in diabetes patients to reduce thirst. However, whether it has a therapeutic effect on T2DM or NAFLD is not known. The aim of this study was to examine whether BHJRST had a lipid-lowering effect using a HuS-E/2 cell model of fatty liver induced by palmitate and in a db/db mouse model of dyslipidemia. Incubation of HuS-E/2 cells with palmitate markedly increased lipid accumulation and expression of adipose triglyceride lipase (ATGL), which is involved in lipolysis. BHJRST significantly decreased lipid accumulation and increased ATGL levels and phosphorylation of AMP-activated protein kinase (AMPK) and its primary downstream target, acetyl-CoA carboxylase (ACC), which are involved in fatty acid oxidation. Furthermore, after twice daily oral administration for six weeks, BHJRST significantly reduced hepatic fat accumulation in db/db mice, as demonstrated by increased hepatic AMPK and ACC phosphorylation, reduced serum triglyceride levels, and reduced hepatic total lipid content. The results show that BHJRST has a lipid-lowering effect in the liver that is mediated by activation of the AMPK signaling pathway.
肥胖及相关病症，如2型糖尿病（T2DM）和非酒精性脂肪性肝病（NAFLD），目前是一个全球性的健康问题。在亚洲传统医学中，白虎加人参汤（BHJRST）被广泛用于糖尿病患者以减轻口渴。然而，其对T2DM或NAFLD是否具有治疗作用尚不清楚。本研究的目的是使用棕榈酸诱导的脂肪肝HuS-E/2细胞模型和血脂异常的db/db小鼠模型，研究BHJRST是否具有降脂作用。用棕榈酸孵育HuS-E/2细胞可显著增加脂质积累和参与脂解的脂肪甘油三酯脂肪酶（ATGL）的表达。BHJRST显著降低脂质积累，增加ATGL水平以及参与脂肪酸氧化的AMP激活蛋白激酶（AMPK）及其主要下游靶点乙酰辅酶A羧化酶（ACC）的磷酸化。此外，在每天两次口服给药六周后，BHJRST显著降低了db/db小鼠的肝脏脂肪积累，这表现为肝脏AMPK和ACC磷酸化增加、血清甘油三酯水平降低以及肝脏总脂质含量降低。结果表明，BHJRST通过激活AMPK信号通路在肝脏中发挥降脂作用。
