Cheon Se-Yun, Chung Kyung-Sook, Lee Kyung-Jin, Choi Ho-Young, Ham In-Hye, Jung Dong-Hoon, Cha Yun-Yeop, An Hyo-Jin
College of Korean Medicine, Sangji University, Wonju-si, Gangwon-do, 26339, Republic of Korea.
Catholic Precision Medicine Research Center, College of Medicine, The Catholic University of Korea, 222, Banpo-daero, Seocho-gu, Seoul, 06591, Republic of Korea.
BMC Complement Altern Med. 2017 Apr 20;17(1):222. doi: 10.1186/s12906-017-1734-z.
HVC1 consists of Coptidis Rhizoma (dried rhizome of Coptischinensis), Scutellariae Radix (root of Scutellariabaicalensis), Rhei Rhizoma (rhizome of Rheum officinale), and Pruni Cortex (cortex of Prunusyedoensis Matsum). Although the components are known to be effective in various conditions such as inflammation, hypertension, and hypercholesterolemia, there are no reports of the molecular mechanism of its hypolipidemic effects.
We investigated the hypolipidemic effect of HVC1 in low-density lipoprotein receptor-deficient (LDLR) mice fed a high-cholesterol diet for 13 weeks. Mice were randomized in to 6 groups: ND (normal diet) group, HCD (high-cholesterol diet) group, and treatment groups fed HCD and treated with simvastatin (10 mg/kg, p.o.) or HVC1 (10, 50, or 250 mg/kg, p.o.).
HVC1 regulated the levels of total cholesterol, triglyceride (TG), low-density lipoprotein (LDL) cholesterol, and high-density lipoprotein (HDL) cholesterol in mouse serum. In addition, it regulated the transcription level of the peroxisome proliferator-activated receptors (PPARs), sterol regulatory element-binding proteins (SREBP)-2, 3-hydroxy-3-methylglutaryl (HMG)-CoA reductase, lipoprotein lipase (LPL), apolipoprotein B (apo B), liver X receptor (LXR), and inflammatory cytokines (IL-1β, IL-6, and TNF-α). Furthermore, HVC1 activated 5' adenosine monophosphate-activated protein kinase (AMPK).
Our results suggest that HVC1 might be effective in preventing high-cholesterol diet-induced hyperlipidemia by regulating the genes involved in cholesterol and lipid metabolism, and inflammatory responses.
HVC1由黄连（黄连干燥根茎）、黄芩（黄芩根）、大黄（掌叶大黄根茎）和郁李仁（郁李树皮）组成。尽管已知这些成分在炎症、高血压和高胆固醇血症等多种病症中有效，但尚无关于其降血脂作用分子机制的报道。
我们研究了HVC1对喂食高胆固醇饮食13周的低密度脂蛋白受体缺陷（LDLR）小鼠的降血脂作用。将小鼠随机分为6组：正常饮食（ND）组、高胆固醇饮食（HCD）组，以及喂食HCD并用辛伐他汀（10毫克/千克，口服）或HVC1（10、50或250毫克/千克，口服）治疗的治疗组。
HVC1调节小鼠血清中总胆固醇、甘油三酯（TG）、低密度脂蛋白（LDL）胆固醇和高密度脂蛋白（HDL）胆固醇的水平。此外，它还调节过氧化物酶体增殖物激活受体（PPARs）、固醇调节元件结合蛋白（SREBP）-2、3-羟基-3-甲基戊二酰辅酶A（HMG）还原酶、脂蛋白脂肪酶（LPL）、载脂蛋白B（apo B）、肝脏X受体（LXR）和炎性细胞因子（IL-1β、IL-6和TNF-α）的转录水平。此外，HVC1激活了5'-腺苷单磷酸激活蛋白激酶（AMPK）。
我们的结果表明，HVC1可能通过调节参与胆固醇和脂质代谢以及炎症反应的基因，有效预防高胆固醇饮食诱导的高脂血症。
