Abstract
BackgroundHVC1 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.MethodsWe 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.).ResultsHVC1 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).ConclusionOur 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.
Highlights
HVC1 consists of Coptidis Rhizoma, Scutellariae Radix, Rhei Rhizoma, and Pruni Cortex
HVC1 regulates lipid metabolism and cholesterol synthesis in high-cholesterol diet (HCD)-fed low-density lipoprotein receptor-deficient (LDLR−/−)mice To investigate whether the lipid metabolism and biosynthesis of cholesterol in HVC1 treated mice was associated with molecular signaling by the genes involved in hyperlipidemia, we examined the expression levels of related genes that are key transcription factors in the liver
5′ adenosine monophosphateactivated protein kinase (AMPK) is a major regulator of energy metabolism, and its phosphorylation is involved in the regulation of adipocyte differentiation [27]; we investigated whether HVC1 regulated energy metabolism through the AMPK pathway
Summary
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). Methods: We investigated the hypolipidemic effect of HVC1 in low-density lipoprotein receptor-deficient (LDLR−/−) mice fed a high-cholesterol diet for 13 weeks. Cholesterol synthesis in the liver is responsive to external factors and suppressed by an increase in dietary cholesterol. Triglycerides and cholesterol both from diet and synthesized in the liver are solubilized in lipoproteins [2]. These lipoproteins contain triglyceride lipid droplets and cholesteryl esters surrounded by polar phospholipids and proteins identified as apolipoproteins. There are Peroxisome proliferator-activated receptors (PPARs) family is nuclear receptors superfamily that regulates in energy homeostasis and metabolic function such as
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