RESUMEN
【Objective】To observe the effect of fucoidan on lipid metabolism enzyme in hyperlipidemia mice.【Methods】Sixty healthy male SD rats were randomized into 6 groups: normal group,model group,gynostemma pentaphyllum(GP,30 mg/kg) group and low-,moderate-and high-dose fucoidan groups(0.1,0.2 and 0.4 g?kg-1 respectively).Except the normal group,the rats in other groups received high fat emulsion(10 mL?kg-1) by gavage to establish hyperlipidemia models.The activities of lipoprotein lipase(LPL),hepatic lipase(HL) and lecithin cholesterol acyltransferase(LCAT) in different groups were compared.【Results】Serum activities of LPL,HL and LCAT as well as hepatic activities of LPL and HL were increased in low-and moderate-dose fucoidan groups.【Conclusion】Fucoidan decreases the serum triglyceride levels by activating the serum and hepatic LPL and HL activities,and decreases serum cholesterol level by activating hepatic LCAT activity.
RESUMEN
Objective To explore the mechanism of Fudoidan for regulating the disorder of lipid metabolism in rats. Methods Rat hyperlipidemic model was established. The effect of Fudoidan on rats levels of blood lipids, lipid metabolic enzyme, and the lipid contents in the stool, as well as bile metabolismand LDL-R mRNA expression in the liver were observed. Results Fudoidan can notably restrain the concentration of serum total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C) of hyperlipidemic rats and increase the concentration of high-density lipoprotein cholesterol (HDL-C) and activities of 1ipoprotein lipase (LPL), hepatic lipoprotein (HL) and lecithin cholesterol acyltransferase (LCAT).Fucoidan can remarkably increase the contents of cholesterol, TG, bile acid , but has no effect on the secretion of bile, the concentration of cholesterol and bile acid in bile. The results of RT-PCR experiment showed that Fudoidan can notably improve the expression level of low-density lipoprotein receptor (LDL-R) mRNA in the liver of hyperlipidemic rats. Conclusion Fucoidan can regulate the disorder of lipid metabolism probably by restraining the absorption of lipids (TC, cholesterol, bile acid) , activating the activities of lipid metabolic enzyme (LPL, HL and LCAT), and promoting the expression of LDL-R mRNA in the liver.