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研究不同分子质量马尾藻岩藻聚糖硫酸酯对高脂血症小鼠体内脂质代谢相关酶和胆固醇合成关键酶的影响。方法:建立高脂血症小白鼠模型,将MMWF、LMWF通过体内实验灌胃小白鼠,测定血清卵磷脂胆固醇酰基转移酶(LCAT)、肝脂酶(HL)、脂蛋白脂酶(LPL)以及肝脏LCAT、LPL活性,研究其降血脂效果。结果:4种岩藻聚糖硫酸酯能显著提高高脂血症小鼠LCAT、HL、LPL活力,降低HMG-COA还原酶活力。与模型组相比,LMWF1和LMWF2各高剂量组小鼠血清LCAT活性分别提高了17.65%,27.21%,10.97%,10.51%;肝脏LCAT活性分别提高了39.73%,43.44%,27.72%和32.22%;血清HL活性分别提高了19.70%,25.76%,8.08%和19.19%;对肝脏HL活力影响不显著;血清LPL活性分别提高了47.16%,51.14%,39.77%和44.89%;肝脏LPL活性分别提高了40.22%,50%,31.52%,36.96%;血清HMG-Co A还原酶活性分别降低了36.70%,38.39%,31.20%和33.59%;肝脏HMG-Co A还原酶分别降低了18.63%,22.07%,14.54%和17.01%。结论:4种马尾藻岩藻聚糖硫酸酯通过促进脂蛋白代谢关键酶LCAT、HL和LPL活性的升高,加快TC和LDL分解代谢;或通过抑制HMG-Co A还原酶,使机体内的TC合成受阻。
To study the effects of different molecular mass of fucoidan on the key enzymes of lipid metabolism and cholesterol synthesis in hyperlipidemic mice. Methods: The model of hyperlipidemia mice was established. MMWF and LMWF were instilled into mice by in vivo experiments. Serum lecithin cholesterol acyltransferase (LCAT), hepatic lipase (HL), lipoprotein lipase (LPL) Liver LCAT, LPL activity, study its hypolipidemic effect. Results: Four kinds of fucoidan sulfate could significantly increase the activity of LCAT, HL, LPL and decrease the activity of HMG-COA reductase in hyperlipidemic mice. Compared with the model group, the serum LCAT activity of mice in each high dose group of LMWF1 and LMWF2 increased by 17.65%, 27.21%, 10.97% and 10.51%, respectively; the liver LCAT activity increased by 39.73%, 43.44%, 27.72% and 32.22% ; The activity of serum HL increased by 19.70%, 25.76%, 8.08% and 19.19% respectively; the effect on hepatic HL activity was insignificant; the serum LPL activity increased by 47.16%, 51.14%, 39.77% and 44.89% 40.62%, 50%, 31.52% and 36.96%, respectively. The serum HMG-Co A reductase activity was reduced by 36.70%, 38.39%, 31.20% and 33.59%, respectively, while the liver HMG-Co A reductase was reduced by 18.63% and 22.07% %, 14.54% and 17.01% respectively. CONCLUSION: Four kinds of Sargassum fucoidan promote the catabolism of TC and LDL by increasing the activities of LCAT, HL and LPL, which are the key enzymes of lipoprotein metabolism, or inhibit the metabolism of HMG-Co A reductase, TC synthesis blocked.