Enteromorpha Polysaccharides Inhibition Of Elevated Blood Lipids Functional And The Preliminary Research Of The Mechanism

Object: The aim of this study was to investigate the hyperlipidemia of enteromorpha polysaccharides,and the preliminary exploration on the mechanism,for the development and utilization of enteromorpha polysaccharides as a health food.Method:1.The adult female SD rats as experimental object,continuous feeding high fat forage35 days to establish hyperlipidemia model.2.The experiment include five groups: Normal group(Normal),Model group(Model),low enteromorpha polysaccharides dose group(low),high enteromorpha polysaccharides dose group(high),positive control group(simvastatin).Normal group was given normal diet;model group,enteromorpha polysaccharides groups,and simvastatin positive control group are high fat feed,five groups are given enough drinking water.Low and high enteromorpha polysaccharides dose groups,respectively with the concentration of 200 mg/kg and 400 mg/kg polysaccharide aqueous solution to fill the stomach every day;Positive control group given simvastatin solution,lavage dose of 20 mg/kg/day;Normal group and model group gastric by distilled water every day.Every 3 days record weight.Tail vein blood total cholesterol(TC),triglyceride(TG)values measured weekly,and record the total food intake.3.At the end of the experiment,determinate the blood TC,TG,high-density lipoprotein(HDL)and low density lipoprotein(LDL-C),alanine aminotransferase(ALT),aspertate aminotransferase(AST),fecal bile acid indicators,Hematoxylin-Eosin staining to observe the liver tissue structure.4.Reverse transcription PCR(rt-pcr)determinated the HMGCR,LDL,SREBP-2,CYP7A1,ACC,SREBP-1 c,FAS mRNA expression level in liver tissue;protein imprinting method(Western Blot)to determinate the SREBP-2,CYP7A1,ACC and SREBP-1 c protein levels.Results:1.In SD rats with established hyperlipidemia,the experiment results show that:enteromorpha polysaccharides can inhibit rat blood fat rise which caused by high-fat diet;compared with blank group,model group's TC,TG,and LDL-C significantly increased(P < 0.05).Compared with model group,low and high CEP dose group's TC,TG,LDL-C significantly decreased(P < 0.05).ALT,AST,and HE staining shows CEP can reduce fat cavitation pathological change in the liver which caused by hyperlipidemia,has certain protective effect on the liver.2.The preliminary mechanism of polysaccharide of enteromorpha inhibit cholesterol increase results show: normal group compare with model group,high fat diet can make HMGCR,LDL-R,SREBP-2,CYP7A1 amount of mRNA expression increase.And compare with model group,enteromorpha polysaccharides and simvastatin drug group decrease amount of mRNA expression of HMGCR,and also the HMGCR protein levels at the same time,the difference have statistically significant(p < 0.05).Compare with model group enteromorpha polysaccharides and drug simvastatin group can cut SREBP-2 mRNA expression,but only the enteromorpha polysaccharides group can reduce the protein levels of SREBP-2(p <0.05).Compare with model group enteromorpha polysaccharides and simvastatin drug group of CYP7A1 mRNA expression has a tendency to decline(p > 0.05),the influence on CYP7A1 protein level has no statistical difference(p > 0.05).Compared with the blank group,high-fat diet groups amount of mRNA expression of LDL-R were reduced(p < 0.05),but no significant differences between groups in terms of a high-fat diet(p > 0.05).3.The preliminary mechanism of enteromorpha polysaccharides inhibit triglycerides increase results show: normal group compare with model group,high fat diet can make the ACC,SREBP-1 c,and FAS amount of mRNA expression increase.And compare with model group,enteromorpha polysaccharides and drug simvastatin group can decrease the ACC amount of mRNA expression(p < 0.05),and at the same time can reduce the protein expression level,and is close to or reached the level ofblank group,the difference statistically significant(p < 0.05).For the amount of mRNA expression of SREBP-1 c: compare with model group,enteromorpha polysaccharides,simvastatin groups have lower expression(p < 0.05),and its protein levels also reduced.For expression of the FAS mRNA: model group compare with blank group has a tendency to rise,but the difference has no statistically significant(p > 0.05).Each dose group compared with model group,had a tendency to cut,but the difference is insignificant(p > 0.05),and simvastatin group compared with model group,the difference was statistically significant(p < 0.05).Conclusion:1.The female SD rats intake of high lipid feed can establish hyperlipidemia.2.Enteromorpha polysaccharides can inhibit high cholesterol,can inhibit the rat caused by high-fat diet of cholesterol and triglyceride levels rise,and also can reduce low-density lipoprotein(LDL)in the serum,has protective function on fatty liver.3.Enteromorpha polysaccharides can inhibit the rat serum cholesterol levels increase caused by high-fat diet,its possible mechanism of action is to make sterol adjust the original binding protein subtype of SREBP-2 the amount of mRNA expression and protein levels are decrease,which makes its downstream genes that speed limit cholesterol synthesis of the key enzymes of HMGCR mRNA expression and protein levels to limit free cholesterol synthesis in the liver,to lower serum cholesterol.4.Enteromorpha polysaccharides can inhibit the rat serum triglyceride levels rise caused by high fat diet and its possible mechanism of action is to make the sterol to adjust the original binding protein subtype of SREBP-1 c amount of mRNA expression and protein levels decrease,and decrease its downstream genes ACC mRNA expression and reduce its protein levels to limit the synthesis of triglyceride in the liver.