| Objective: To investigate the protective effect of compound flavonoids on atherosclerosis in ApoE knockout mice.Methods: seven-week old ApoE-/-mice(n=75)were fed with high-fat diet and were assigned randomly into 5 groups: Model group,Simvastatin group,Low compound flavonoids group(200mg.kg-1),Middle compound flavonoids group(400mg.kg-1),High compound flavonoids group(800mg.kg-1).seven-week old C57BL/6 mice considered of the normal group(n=15).After 16 weeks,serum,aortas and liver from mice were harvested.Serumlipids,superoxide dismutase(SOD)activity,NF-k B and IL-1 b in serum were detected.The levels of lipids,SOD,MDA in liver were determined.Pathological changes of liver and vessels were observed by H-E and Oil red O staining.The related proteins expression were detected by Western Blot.Results:1.Diet was normally taken,the average body weight of the model group was the heaviest in mice,and the body weight in normal group was the lightest.2.The atheromatous plaquewere observed in aortic with H-E and oil red O staining.The size of plaque were significantly decreased in model group with medium concentration of flavonoids treatment and model group with high concentration of flavonoids treatment.3.The expression of IL-1 b and NF-k B in the compound flavonoids group was significantly lower than that in the model group(P(27)0.05).4.The level of TC,TG,LDL-C in serum and liver in model group with flavonoids treatment were significantly lower than the model group,while the serum HDL-C were higher(P(27)0.05).The level of SOD in Serum and liver increased remarkably,but the MDA decreased(P(27)0.05).5.The severe hepatic steatosis in the model group was found,but it was ameliorated through treatment with flavonoids.Compared with the model group,the expression ofAMPK phosphorylation and PPAR gamma in the liver was remarkably up-regulated via treatmen to flavonoids(P(27)0.05).Conclusion: The flavonoids may decrease the development of atherosclerosis in mice by regulating blood lipid,inhibiting inflammation and anti-oxidation.This may be involved in the up-regulation of AMPK phosphorylation and PPAR gamma to regulate live lipid metabolism. |