Abstract
Mechanisms of the water extracts of Polygoni Multiflori Radix (PMR) and its processed products (PMRP) on liver lipid metabolism were observed in this paper. Aqueous extract of PMR and PMRP was given to nonalcoholic fatty liver model rats, respectively. PMR was better in reducing the contents of very low density lipoprotein (VLDL) than PMRP and the positive control groups. In the aspect of regulating TG, medium dose PMR reduced the activity of diacylglycerol acyltransferase (DGAT) to 1536 ± 47.69 pg/mL (P < 0.001) and promoted the expression of hepatic lipase (HL) to 23.59 ± 0.2758 U/mL (P < 0.05). HL promotion ability of medium dose PMR was similar with the simvastatin positive control. Both medium and high dose of PMR showed significant alterations in TC, which were related to the downregulation effects on hydroxyl methyl-glutaryl coenzyme A reductase (HMGCR) and upregulation effects on cholesterol 7-alpha-hydroxylase or cytochrome P450 7A (CYP7A). Quantitative relationships research indicated that the prominent effect on inhibiting the content of HMGCR (r = 0.756, P < 0.05) was strongly positive correlated with to the TC regulation effects. Effects of PMR on enhancing decomposition rate or reducing de novo synthesis rate of TG and TC were better than PMRP.
Highlights
Fatty liver disease (FLD), a kind of lipid metabolic disorder of liver, is a reversible condition in which large vacuoles of triglyceride fat accumulate in liver cells via the process of steatosis
According to the different inducements of fatty liver, FLD is divided into alcoholic fatty liver disease (AFLD) and nonalcoholic fatty liver disease (NAFLD)
NAFLD is increasingly recognized as the hepatic manifestation of insulin resistance and the systemic complex known as metabolic syndrome [1, 2]
Summary
Fatty liver disease (FLD), a kind of lipid metabolic disorder of liver, is a reversible condition in which large vacuoles of triglyceride fat accumulate in liver cells via the process of steatosis (abnormal retention of lipids within a cell). In NAFLD pathogenic process, the accumulation of lipid within the liver, especially total cholesterol (TC) and triglycerides (TG) accumulation, has been confirmed by dynamics research. These researches point out that TC, TG, and esterification of free fatty acid (FFA) accumulation in the liver for the treatment of NAFLD might have direct influence [7, 8]
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